Bernard Gesch is a senior research scientist in the

Transcription

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Bernard Gesch is a senior research scientist in the Department of Physiology, University of
Oxford. He is also the director of the research charity, Natural Justice, which investigates
causes of antisocial and criminal behaviour. This chapter is dedicated to the memory of
Bishop Hugh Montefiore, inspirational Chairman of Natural Justice.
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Chapter 7*
The potential of nutrition
to promote physical and
behavioural well-being
Bernard Gesch
Introduction
Good nutrition is considered to be seminal to our physical well-being throughout
our lives. It is widely accepted as a major factor in the prevention of chronic disease.
Since the brain also has to be nourished, there are increasingly good reasons
to believe that the health benefits of good nutrition extend into positive effects
on our behaviour.Yet it is curious that most of the authoritative reference works
on diet and international dietary standards focus on health issues but hardly
mention behavioural well-being. It is argued that such standards should be
reassessed to take into account brain function and behaviour.
Food is a meeting point of the social and physical worlds.The availability of food,
food types, and food choices will interact with a wide range of socio-economic
factors.Yet, no species can flourish without food and water.This global necessity
highlights vast inequalities. Many of the World’s population starve while at the
same time we are witnessing an epidemic of obesity.This may be the visible tip of
an iceberg and, to extend that analogy further, it is the 90% that goes unseen below
the water that is the most dangerous.The impacts of various changes in modern
diets such as increased intakes of salt, saturated fats, and refined sugars are already
apparent in global health.This chapter will extend the discussion to examine the
relationship with behavioural well-being.
The nutritional ascent of man
The human brain is exceptionally large for a terrestrial animal and has facilitated
an enhanced capacity for adaptation and problem-solving (Crawford et al. 1999).
Anthropological science has taught us how important nutrition was during the
evolution of our brain (e.g. Martin 1983; Blumenschine 1991; Foley and Lee
1991).The brain is a fatty organ and it is believed that the availability of two highly
* © Bernard Gesch 2005
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unsaturated fatty acids, arachidonic acid (AA) and docosahexaenoic acid (DHA),
from which our central nervous system is primarily constructed is likely to have
been a limiting factor in brain size (e.g. Crawford et al. 1972; Broadhurst et al. 2002)
and complexity (Fernstrom 1999).The omega-3 highly unsaturated fatty acids that
are most important for brain function, eicosapentaenoic acid (EPA) and DHA, are
only found in appreciable quantities in oily fish and seafood, primarily because
these creatures consume the algae that synthesize EPA and DHA. The dietary
omega-3 precursor of EPA and DHA is alpha-linolenic acid (ALA). It is found in
dark green leafy vegetables and some nuts and seeds, but its conversion to DHA in
particular may be limited (Burdge and Wootton 2002). AA on the other hand is an
omega-6 fatty acid and this group is plentiful in modern diets. Omega-6 fatty acids
are typically found in vegetable oils, but AA is found in meat and dairy produce.
The fact that the savannah is not a rich environment for DHA has led scientists to
reconsider whether Homo sapiens really did evolve on the plains (Broadhurst et al.
2002; Crawford et al. 1999) rather than near water in coastal or lakeside habitats
(Stringer 2000; Tobias 2002; Morgan 1990). However, DHA could have come from
eating the fresh brains of other terrestrial animals on the savannah. So, either
humans used their stone tools to break open the strong skulls of freshly slaughtered
beasts, or they could have simply reached down on the shore and popped fresh
shellfish into their mouths; for an intelligent species the latter has greater elegance.
Certainly, some of the earliest fossil remains of our species have been found on the
shoreline of the Cape of Good Hope (Stringer 2000; Rightmire and Deacon 1991)
and it is gaining credence in anthropology that it was around coastal and inland
shorelines that our brain mass evolved to about twice the size of that of our
predecessor, Homo habilis (Crawford et al. 1999; Broadhurst et al. 2002).
The evolution of such a metabolically expensive organ is remarkable because in
the adult it consumes around 20% of available energy (Leonard and Robertson
1997) and receives 12% of basal cardiac output to supply it with nutrients
(Shepherd et al. 1983). A recent article concluded that middle Palaeolithic people
(Neanderthals) were less effective at exploiting coastal and lakeside food resources
than Homo sapiens in the upper Palaeolithic era (Klein et al. 2004).This change in
exploitation occurred as recently 50 000 years ago and it is argued this may have
been the decisive change in our behaviour that facilitated our success over
Neanderthals (Klein et al. 2004). Furthermore, it has been pointed out that, in
coastal hunter–gatherer cultures, women tend to collect shellfish and this may have
been true of our ancestors as well (Parkington 1998). A pregnant mother would
thus have ready access to large quantities of the nutrients essential for the development of her fetus’s brain and central nervous system, which receives 70% of the
energy supplied (Cunnane et al. 2000). Shellfish are also a rich source of protein
and animal studies have demonstrated that lower maternal protein intakes reduce
delivery of DHA from the mother to the fetus, which may impair the development
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NUTRITION TO PROMOTE PHYSICAL AND BEHAVIOURAL WELL-BEING
and function of the fetal brain (Burdge and Wootton 2002). Klein and colleagues
(2004) suggest that the Palaeolithic evidence points to the collection of shellfish
as the key source of nutrients rather than deep water fishing as there is a lack of
evidence for fishing technology. Certainly, it appears to be the case that shellfish
were plentiful in the areas where early fossils of our ancestors have been found
(Stynder et al. 2001).
Moving into the fast lane
It should be recognized, however, that anthropology is an uncertain science involving
the meticulous piecing together of evidence to form a picture, but many of the
conclusions about the importance of nutrients on brain development are beginning
to be supported by experimental evidence, indicating that nutrients rich in sea food
are as relevant to brain development now as they appear to have been to our
forebears (Uauy et al. 2001). Indeed, shellfish not only supply DHA and EPA but are
also particularly rich in trace elements such as zinc, iron, and iodine when compared
to deep-water fish.These nutrients are also essential for cognitive development, offering further support to anthropological evidence that these were the food sources
that facilitated our brain development. Zinc, for instance, may also turn out to be
limiting factor in brain development as intake positively correlates with fetal head
circumference (Ward et al. 1990) and has been shown experimentally to alter essential
fatty acid composition (Wauben et al. 1999;Ayala and Brenner 1983, 1987; Dieck et al.
2005).Animal studies have shown that that low zinc (Oteiza et al. 1990) and also low
protein intakes (Bennis-Taleb et al. 1999) impair brain development. Fortunately for
us, our highly evolved brain appeared to pay off as evidence suggests our ancestors
moved north and overwhelmed existing populations of Neanderthals (Klein et al.
2004). Indeed, contemporary findings from 10 of 13 randomized trials suggest that
significant improvements occur in nonverbal intelligence when participants are given
micronutrient supplementation (Benton 2001) but these effects depend on the
quality of dietary baselines; broadly the worse the diet, the greater the effect. In a
population of rural Thai children where zinc, iron, and iodine deficiencies are
prevalent, supplementation of these nutrients treated the deficiency with concomitant
improvements in cognitive functioning (Manger et al. 2004). Since nutrients appear
to positively impact cognitive functioning nowadays, it is feasible that better nutrition
raised our ancestors’ functioning to a new level.
Food for thought
An underlying question remains as to which is the causal factor.Thus, did our diet
actually shape our behaviour, was it the other way round, or, indeed, a little of
each? The environment in which a living organism evolved is likely to have been
a determinant of which elements became essential for life. The phospholipid
membrane structure of the brain, as well as the use of trace elements as enzyme
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catalysts, is considered to have originated in a marine environment (Broadhurst
et al. 2002; Nielsen 2000).This is consistent with evidence that is suggestive that a
coastal diet provided a suitable nutritional environment to support the physical
enlargement of our brains.While nutrition is widely accepted as influencing longterm health, we somehow manage to decouple that relationship from behaviour
with the assumption that our behaviour is purely a matter of free will. This is
despite the fact that we cannot by any means decouple nutrition from actual brain
function.
Nevertheless, Derek Bryce-Smith in his Royal Society of Chemistry Lecture
(Bryce-Smith 1986) reviewed evidence that poor nutrition or exposure to lead
(a neurotoxin and nutrient antagonist) might influence behaviour, personality, and
mentation. He reasoned that, since nutrients support the operation of our senses, an
individual couldn’t normally sense a lack of nutrients or exposure to neurotoxins
ambient in the environment. Hence, Bryce-Smith proposed that there could be
potent effects on our behaviour that (unlike alcohol) act without our knowledge,
e.g. an association between exposure to lead and violence (Needleman et al. 1996;
Masters 2000; Stretesky and Lynch 2001). Essential nutrients are involved in protecting the body from the deleterious effects of neurotoxins. Furthermore, if an
individual is unwittingly undermined by poor nutrition, those around them are
unlikely to know about it either, and would tend to attribute any inappropriate
behaviour to deficits in the perpetrator’s personality.
Changing dietary baselines
If this scenario is correct, our forebears’ diet may have been a recipe for success.
Curiously then, there is surprisingly little overlap between estimates of what our
ancestor ate and what we eat nowadays: the intakes of the essential omega-3 and
omega-6 fatty acids were 1:1 rather than the 1:15 ratio found nowadays, perhaps
the most extreme example of dietary change (Eaton and Konner 1995; Eaton
and Eaton 2000; Eaton et al. 1997): Palaeolithic diets are considered to provide
more fibre and less salt; carbohydrates would come chiefly from uncultivated
vegetables, fruit, and perhaps honey rather than the grains and refined sugar
consumed nowadays. The focus of further discussions will be on these dietary
factors.
There are, however, many other factors in addition. We can be sure that our
ancestors did not eat a highly processed diet.The Palaeolithic diet would probably
have provided more phytochemicals, which we are beginning to appreciate are
also important for health (Eaton and Eaton 2000). Palaeolithic diets would, by current standards, be considered organic, additive- and pesticide-free (Curl et al. 2003;
Egger et al. 1985; Schab and Trinh 2004). Our forebears are likely to have expended
more energy in physical activity (Eaton and Eaton 2003), and we are well aware
that sedentary lifestyles are associated with obesity and undesirable consequences
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for health (US Department of Health and Human Services 1996;WHO 1998).
Diet also interacts with our genes (see Simopoulos and Pavlow 2001).
While we cannot be certain of the Palaeolithic diets and estimates have been
revised over the years, it would nevertheless be prudent to test experimentally the
relative merits of modern diets with such differing dietary baselines—particularly
as it is argued that our genes are attuned to the Palaeolithic diet (Cordain et al. 2000).
How quickly can we expect our brain to adapt to its new nutritional environment?
Perhaps our forebears were so closely engaged in the collection of food that they
never took food security for granted. Indeed, it is useful to reflect if it is the hallmark of an intelligent primate that we are only now recognizing the seminal role of
the aquatic environment for our well-being, just as concern is growing about the
exhaustion of fish stocks through wasteful overexploitation (Clover 2004) and the
contamination of fish stocks (Hightower and Moore 2003) through ill-considered
treatment of the world’s oceans by industrialized nations.
Organized food production
We may be tempted to look back to our hunter–gatherer origins through rosetinted glasses, but the increased security of food availability from agriculture and
industrialization is likely to have facilitated the expansion of our population.
If food shaped our behavioural strategies about 50 000 years ago, then it seemed to
happen again around 10 000 years ago when we began organizing our society
around agricultural food production, which played an important role in shaping
our present social structures and higher population densities (Crawford et al. 1999).
Curiously, despite the likely advantages of better food security, it is argued that
this change in food harvesting may have resulted in a decline in life span from
that of the hunter–gatherer (Angel 1984).This could well be related to increased
population density and the spread of infectious diseases. It is also possible that
another element was the change in diet. Comparisons of active wild animals
with farmed animals illustrate important changes in body tissue composition.Wild
animals contain a higher percentage of protein than farmed animals (15% versus
10%) and a lower percentage of fat (5% versus 30%). Fat provides 9 calories for
every gram consumed, so the wild animal would provide only 45 calories as fat to
every 270 calories as fat from the extensively reared animal (Crawford 1968).The
types of fats also differ (e.g. Ledger, 1968; FAO 1994). In wild animals the ratio of
non-essential to essential fatty acids is typically 3 to 1, whereas in modern beef the
same ratio is reported to be 50 to 1 (Crawford 1968). Animal studies have also
shown that both nutrient restriction and overnourishment during pregnancy suppress placental cell proliferation and vascularity, which has an important impact on
fetal development and thereby on neonatal mortality and morbidity (Redmer et al.
2004). Indeed, estimates of life span based on that of modern hunter–gatherers are
around 40 years of age, whereas life expectancy from the onset of agriculture was
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estimated to be relatively stable at around 20–25 years until the onset of industrialization in about 1800 (Eaton et al. 2002a, b).
The dawn of dietary complacency
A major benefit of industrialization appears to have been the extension of life
expectancy.This is generally attributed to better food security and sanitation.There
is, however, a possible downside, as incidence of degenerative disease increased.
Longer life expectations and lack of exercise doubtless contributed to this, but the
link with dietary change is also strong. As our social structures became more
sophisticated,Westernized countries became increasingly distant from our food
supplies. Most recently, with the globalization of markets, we may have surrendered
control to the food industries. In the process, we seem to have forgotten that food
and water are the physical basis for our survival.
With the onset of industrialization from around 200 years ago, it seems, from the
perspective of what we eat, that a miracle must have occurred, because, irrespective
of how much salt, saturated fat, hydrogenated fats, and refined sugar we started eating,
we seemed to assume it had no implications for our well-being.Was this the ascent
of man from primordial soup to the couch potato? Can it really be assumed that
our nutrition was crucial in our evolution but has no relevance now? Or could
something as simple as paying more attention to what we eat potentially be a
major resource in promoting human well-being?
Diet and physical well-being
Food inequality in developing countries
No species can flourish without adequate food and water. Sadly, for many of the
world’s population, this is the cruel reality as, according to the UN Food and
Agriculture Organization (FAO 2003) report, there were 840 million people in the
world who did not have enough to eat.The laudable target set at the millennium
World Food Summit to halve global hunger by 2015 is already off target and,
according to the FAO, the present rate of decline of hunger will need to
be increased 12-fold to reach that target (FAO 2003). Indeed, the overall decrease
in global hunger is largely due to improvements in China. The scale of the
Chinese achievement obscures the fact that hunger has got worse in 47 countries
(Short 2002).
Diet-related low birthweights affect approximately 30 million children born each
year, which has implications for their mental and physical development as well
their survival (WHO 2002; de Onis et al. 1998) and chronic diseases later in life
(e.g. Barker 1995; Barker et al. 1989, 2001). For the two-thirds of the world’s absolute
poor who still do not have food security, there is an irrefutable case that better food
would promote their physical and social well-being.The hunger of these people
puts our global economic culture into perspective. How precious even the most
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humble offer of food and water must appear when faced with such tragic circumstances. The World Health Organization (WHO) has published perhaps the
definitive studies on changes in global dietary practices and, according to the
WHO (2003, section 2.2),
Hunger and malnutrition remain among the most devastating problems facing the majority of
the world’s poor and needy people, and continue to dominate the health of the world’s poorest
nations. Nearly 30% of humanity is currently suffering from one or more of the multiple forms
of malnutrition (WHO 2000).The tragic consequences of malnutrition include death, disability,
stunted mental and physical growth, and as a result, retarded national socioeconomic development.
Some 60% of the 10.9 million deaths each year among children aged under five years in the
developing world are associated with malnutrition.
If the anthropological perspective on our dietary origins is correct, it could be
predicted that patterns of nutritional deficiencies seen nowadays would be related
to our movement away from our historic coastal and lakeside food sources. It is
noteworthy that the most important nutrient deficiencies globally are nutrients
that are typically richest in shellfish and seafood. Iodine deficiency is estimated to
affect more than 700 million people and is considered the greatest single preventable
cause of brain damage and poor cognitive function (WHO/UNICEF 1999;
Driutskaia and Riabkova 2004). It is estimated that 250 million young children are
affected by subclinical vitamin A deficiency, which is considered the greatest
preventable cause of childhood blindness and increased risk of infections and death
(WHO/UNICEF 1995). Over 2000 million people are estimated to suffer from
anaemia (WHO/UNICEF 2001). Unfortunately, dietary standards have only
recently considered deficiencies in fatty acid intake and its sequelae.
In addition to food insecurity, many developing countries are experiencing rapid
changes from traditional diets.These changes typically reflect trends towards Western
dietary practices of high saturated fat and energy-dense foods. Increasingly,
malnourishment persists with rapidly emerging incidence of chronic disease
attributed to modern diets—so much so that by 2020 it is projected that, in the
developing countries, diet will account for 71% of mortality from ischaemic heart
disease and 75% of deaths due to stroke. Diabetes is projected to increase from 84
million in 1995 to 228 million in 2025 (Aboderin et al. 2001). On a global basis,
60% of the burden of chronic diseases will occur in developing countries.
If there are ways of ensuring that the typical circumstances of an entire population
can be induced to favour distinctly positive health, surely finding a more equitable
method of food distribution must be among them.
Food excess in Western countries
Western diets in particular have increasingly focused on energy-dense foods like
saturated fats and sugar. According to the WHO (2003), ‘the increasing
Westernization, urbanization, and mechanization in most countries around the
World is associated with changes in diets towards one of high-fat, high-energy
foods and sedentary lifestyles.’
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Obesity
Obesity is a function of both energy intake and exercise but the evidence linking it
to energy-dense foods is compelling. For instance, a meta-analysis of 16 studies
testing high-fat versus low-fat diets concluded that a 10% reduction in fat intake
over typically 2 months resulted in a loss of around 3 kg in body weight (Astrup
et al. 2000). Similarly, consumption of energy-dense sugary drinks is associated with
increased weight when examined by cross-sectional, longitudinal, and cross-over
studies (Tordoff and Alleva 1990; Harnack et al. 1999; Ludwig et al. 2001). China
has just reported that the numbers of obese people in its population has doubled
to 60 million between 1992 and 2002, almost equalling the numbers in America in
10 short years. Obesity and depression have been reported as a major factor in
maternal death in Britain (Brettingham 2004). Even economically poor countries
are witnessing a disturbing increase in incidents of childhood obesity (de Onis and
Blössner 2000).The best known comorbidities of obesity are diabetes and heart
disease.
Diabetes
Diets high in saturated fats are an important risk factor for diabetes (Tuomilehto
et al. 2002; Knowler et al. 2002). Australian Aboriginals have an inherent tendency
to insulin dependence but this only seems to manifest itself when they consume
Western diets (O’Dea 1991).
Cancers
WHO (2003) estimates that only a negligible proportion of the world’s population
consumes the recommended intakes of fruit and vegetables, which is an important
part of dietary variation. Diet is estimated to account for 30% of cancers in industrialized countries (Doll and Peto 1996) and 20% in developing countries (Willet
1995). Epidemiological studies provide circumstantial evidence that incidence of
cancers follow the nutritional transitions of Latin America, Africa, North America,
and Asia (Popkin et al. 1993).
Heart disease
Evidence of the role of saturated animal fats in cardiovascular disease is strong and has
been demonstrated in animal experiments, epidemiological studies, and clinical trials
in various populations (Kris-Etherton P et al. 2001). Heart rate variability is considered to be a good indicator of heart condition where beat-to-beat variations of
heart-beat are measured using spectral estimation techniques (DePetrillo et al. 1999).
Lowered heart rate variability has been associated with major depressive disorders
(Carney et al. 1995;Tulen et al. 1996), minor depression (Carney et al. 1995), and
‘depression self-rating’ in non-depressed subjects (e.g. Krittayaphong et al. 1997).
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Processed foods
Other aspects of modern processed diets have also been found to be highly
questionable from a health perspective such as trans fatty acids from the industrial
hardening of oils and increasingly from high-temperature fried foods.This process
introduces hydrogen into polyunsaturated oils, resulting in a more extended fatty
acid carbon chain similar to that of saturated fatty acids.This de-odorizes the oil
and improves shelf life: qualities that are attractive to the food industry.
Unfortunately, there is no evidence to suggest any health benefits from consuming
trans fatty acids—quite the contrary. Since the early 1990s evidence has suggested
that trans fats adversely affect fetal and infant growth by interfering with the
biosynthesis of AA and DHA, the main structural fats in the central nervous
system (Koletzko 1992; van Houwelingen and Hornstra 1994) and more recently
in preschool children (Innis et al. 2004).Trans fats have also been shown to increase
the rate of heart disease in large cohort studies (Oomen et al. 2001;Willett et al.
1993).The US Food and Nutrition Board (2002) famously suggested a ‘tolerable
upper intake level’ of zero! High sodium intake is also a matter of concern in
Western diets as a major risk factor associated with high blood pressure.This
relationship has been demonstrated experimentally, by epidemiological studies,
controlled clinical trials, and in population studies on restricted sodium intake
(Gibbs et al. 2000).
The positive benefits for health of better diets
The positive flip side of this evidence implies that eating a better diet would be protective from these chronic diseases and certainly that would be the position argued
by WHO. A meta-analysis of 32 trials (Cutler et al. 1997) concluded that a daily
reduction of sodium intake reduced systolic and diastolic blood pressure in those
with high blood pressure. For instance, studies that reintroduced dietary factors that
would be plentiful in the Palaeolithic diet, such as fish oils and vitamin E, found
a reduction in mortality by cardiovascular disease of 30% after a 3.5 year follow-up
(GISSI-Prevenzione investigators 1999). Fish consumption correlates as a protective
factor against chronic diseases in China (Wang et al. 2003). Double-blind placebocontrolled clinical trials of omega-3 fatty acids have demonstrated improved heart
rate variability of adult subjects given fatty acids during 24-hour monitoring
(Christensen et al. 1996, 1997, 1999). There is evidence that fish oils provide a
protective effect in certain groups of cancers such as breast cancers (Palakurthi et al.
2000), an illness that is more common in industrialized countries. Numerous studies
have shown that the consumption of fruit and vegetables, and in some cases pulses, is
protective against cancers (World Cancer Research Fund 1997). Zinc supplementation has been shown in a double blind trial to reduce childhood mortality in small
for gestational age infants (Sazawal et al. 2001).
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A need for balance
If we are seeking to raise many of the world population from the shadow of
chronic disease to distinctly positive health, then it is arguable that finding a
dietary middle-way between the extremes of starvation and excess should be a
priority.
Healthy food choices
At the same time that there is concern that we are eating too much sugar and
saturated and trans fats, we also do not seem to be eating enough of the healthy
foods such as fruits and vegetables. According to the US Centers for Disease
Control (CDC 2002), for instance, 79% of US high school students had eaten less
than the recommended five servings of fruits and vegetable a day.
Even the nutritional qualities of the healthy staple foods may also have altered.
A comparison (Mayer 1997) of the nutritional values of fruit and vegetables first
published in 1936 in the seminal work, The nutritive value of fruits, vegetables and
nuts (McCance et al. 1936), with revised figures published in the fifth edition
(Holland et al. 1991) showed there was significantly less calcium, magnesium,
copper, and sodium in vegetables and magnesium, iron, copper, and potassium in
fruit.The reason given for the update was because ‘the nutritional value of many
of the more traditional foods has changed’. A comparative study highlighted
changes to national diets in the UK in the last 50 years. A comparison of diets
consumed by 4599 4-year-old children in 1950 was made with 493 children from
the 1992/93 National Diet and Nutrition Survey.The authors (Prynne et al. 1999)
concluded that the post-war diet, with its reliance on staple foodstuffs such as
bread and vegetables, might well have been beneficial to the health of young
people.Thus, the increase in food choice we hold dear nowadays may not necessarily be beneficial from a nutritional perspective.With the availability of such a
variety of healthy foods to choose from today it is intriguing to consider why we
do not manage to make better food choices. A possible answer is that, typically, it
is the energy-dense foods that are often heavily promoted so perhaps this is driven
by conscious choices. After all, the food industry has invested a great deal of effort
in packaging foods to be attractive (Nestle 2003). Nestle (2002) characterises the
food industry claims as ‘there is no such thing as good or bad food [except when
their products are considered good]’.Alternatively, it has been proposed that energy
density influences energy intake due to weak satiety signals that fail to compensate for very energy-dense foods (Prentice and Jebb 2004). It could be a matter of
taste. Our sense of taste is influenced by zinc status for instance (Bryce-Smith and
Simpson 1984). The addition of sugar, salt, and fats results in very stimulating
foods that may be more palatable if the sense of taste is less sensitive. A survey
found that only 56% of the US population had adequate zinc intakes (Breifel et al.
2000). According to the International Bibliographic Information on Dietary
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Supplements (IBIDS) database of the Office of Dietary Supplements (ODS) at the
National Institutes of Health, 98% of zinc is removed when sugar is refined, a
common feature of modern dietary practices.
Another possibility is that high fat and sugar diets influence our brain chemistry
directly and may have addictive qualities. While researching factors in obesity,
animal studies suggest that mu opioid stimulation enhances the appetite for high
fat and sugar consumption (Zhang and Kelley 2000) and vice versa. High glucose
intakes of 25% added to feeding chow (Colantuoni et al. 2001) have been shown to
stimulates mu-1 and dopamine D1 receptors much like drugs of abuse. It is argued
that there may be a genetic adaptation towards energy-dense foods that developed
at a time before we had unlimited supplies of these foods (Kelley et al. 2002).When
animals are intermittently withdrawn from sugar intakes of 25% they exhibit signs
of withdrawal (Colantuoni et al. 2002). So far, such findings do not seem to have
been replicated on human populations. Nevertheless, breakfast cereals can contain
40% sugars and some drinks contain 100% of calories as free sugars.
This brings us back to the disparity between the estimates of the Palaeolithic diet
where free sugar intakes are estimated to be far lower than in modern times. If our
physiology and genetic make-up is more fully adapted to the diet of the last 50 000
years rather than that of the last 200 years as has been suggested (Cordain et al.
2000), we need to take notice, because our dietary baselines seem to have shifted
considerably. These changes may map out into our behaviour. Following the
publication of the US Food and Nutrition Board statement (2002) suggesting
that we minimize consumption of trans fats, evidence has emerged from an animal
study that dietary trans fatty acids may act on the endogenous neurotransmitter
levels during brain development (Acar et al. 2002). Since these same neurotransmitter
pathways are also implicated in mental illnesses such as schizophrenia (Davis et al.
1991), we are presumably left to guess if the introduction of trans fats has similarly
affected human brains and if there are any consequent mental health implications.
The fact is we don’t know and it should be a concern that evidence emerges after the
widespread introduction of such dietary changes.Are the improved keeping qualities
of hydrogenated oils really a good trade-off for the functionality of our brains?
While the adoption of such unhealthy food products is doubtless profitable,
perhaps it would be a good idea to systematically test new food types for their
implications on our brains before introducing them.
Diet and mental health
It is curious that many of the authoritative reference works on diet and international dietary standards focus on the health issue but hardly mention mental health.
Unless we still believe that mind and body are separate, we might expect that what
we eat would influence brain function if only because of its high metabolic activity.
The blood–brain barrier protects the brain’s nutrient supply, but it is not invulnerable.
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Animal studies suggest that the brain’s composition does not change as quickly in
response to diet as the liver for instance, but smaller changes were noted nevertheless (Crawford et al. 1976). Many of the nutrients supplied to the brain are classed
as essential. Indeed, diseases of nutritional deficiencies such as pellagra can present
as mental confusion and delusions that can give the appearance of mental illness.
Increasingly, there are good reasons to believe that the health benefits of good
nutrition extend into effects on mental health.This brief discussion will touch on
some of the evidence that nutrients can also positively impact on mental illness,
perhaps holding out the possibility of a degree of prevention in the future.
Patterns of mental illness appear to be similar to the cross-national patterns of
chronic disease in that, broadly, they are increasing in prevalence and appear to follow
modern dietary practices, but it is recognized that we are only gradually beginning
to appreciate what is a very complex picture.
Depression
A multinational epidemiological study that examined incidents of depression and
schizophrenia found strong correlations with national dietary practices (Peet 2004).
The most striking finding was that sugar consumption was strongly associated with
worse outcomes in schizophrenia and prevalence of depression, while fish consumption was inversely associated with depression. Like any epidemiological data,
these findings have to be interpreted with care. Such data cannot demonstrate a
causal relationship but the strength of the correlations does, nevertheless, strongly
suggest a need for follow-up clinical trials. Evidence is converging from treatment
studies to indicate that the same nutrients that would have been plentiful in
estimated Palaeolithic diets are protective against depression.The fish oil EPA was
found highly effective in a case of severe treatment-resistant depression (Puri et al.
2001, 2002) and randomized controlled trials have confirmed that it can significantly reduce symptoms of unipolar depression (Nemets et al. 2002; Peet et al.
2002) and similar benefits have been found for omega-3 treatment in bipolar
mood disorder (Stoll et al. 1999). Peet demonstrated that a one-gram dose of EPA
was more effective than a larger dose (Peet and Horrobin 2002) in treating depression in patients who remained depressed despite adequate medication.This suggests
that there are optimal dosages, which is reassuring from an evolutionary perspective as moderate intakes are more easily achievable on a daily basis. In addition to
consuming less omega-3 fatty acids nowadays, it has also been noted that we may
not eat sufficient green vegetables, a good dietary source of folate (Gerrior and
Zizza 1994).There is strong evidence of the protective relationship between folate
intake and depression, as set out in a Cochrane review (Taylor et al. 2003).A number
of clinical studies have found low zinc status in depressed patients compared to
controls (e.g. Maes et al. 1994, 1997; McLoughlin and Hodge 1990). Furthermore,
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the severity of unipolar depression was negatively correlated with the serum level
of zinc. A pilot randomized controlled trail of 14 patients with unipolar depression
on antidepressant medication found that those who received 25 mg zinc daily
significantly augmented the reduction in Beck Depression Inventory (BDI) scores
by 40% after 12 weeks of treatment when compared with placebo supplementation
(Nowak et al. 2003).The authors appropriately argued that this should be followed
up with larger trials.
Schizophrenia
There is a history of treating schizophrenia with various dietary interventions
but, sadly, this has received little attention until comparatively recently. Within
schizophrenia there is considerable heterogeneity, so there is a need for caution in
generalizing about this condition but abnormalities of fatty acid and phospholipid
metabolism have been consistently reported, including excessive activity of PLA2
enzymes, increased lipid peroxidation, and nuclear magnetic resonance (NMR)
spectroscopy evidence of increased brain membrane phospholipid turnover (Peet
et al. 1999). Controlled trial treatments with omega-3 fatty acids have been shown
to be effective in reducing hallucinations and delusions as well as anhedonia,
inattention, or lack of volition, in both medicated and unmedicated patients (Puri
et al. 1998; Peet et al. 2001). In patients given 2 g/day EPA there were improvements on the positive and negative affect scale (PANAS) and its subscales, but there
was also a large placebo effect in patients on typical and new atypical antipsychotics
and no difference between active treatment and placebo. In patients on clozapine,
however, there was little placebo response, but a clinically important and statistically significant effect of EPA on all rating scales.This effect was greatest at 2 g/day
rather than at a higher dose of EPA (Peet et al. 2002).This suggests that there are
optimal dosages and that nutrients can augment the effectiveness of drugs. Clinical
improvements following treatment with EPA have also been shown to correlate
with improved blood fatty acid status, reduced membrane phospholipid turnover,
and reversal of cerebral atrophy (Puri et al. 2000; Richardson et al. 2000). Negative
results have been reported in only one of five controlled trials to date where a
3 g/day intervention was used (Fenton et al. 2001).These data on fish oils indicate
that it is EPA rather than DHA that is effective but it has to be recognized that
these are relatively small studies and more large-scale clinical trials are required,
particularly as this is a low-risk approach.
Overall, these findings are highly encouraging but a great deal more research is
needed in this area, particularly focusing on the possibility that a better diet is
protective from such illness.The World Health Organization is predicting a 50% rise in
child mental disorders by 2020.This strongly suggests that the relationship between
diet and mental health should be added to formal considerations of dietary adequacy.
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Nutrition and behavioural well-being
It may be possible to extrapolate from the health benefits of diet to our behaviour.
The primary concern will be to focus on the possibility that diet can influence
behaviour directly and hence that dietary interventions may even be possible for
behavioural disorders.
Childhood developmental disorders
Evidence is emerging that diet may be linked with childhood developmental
disorders. Many of the features associated with attention deficit hyperactivity
disorder (ADHD), dyslexia, dyspraxia, and autistic spectrum disorders are consistent
with lack of or imbalances in highly unsaturated fatty acids (Richardson and Ross
2000). Fatty acid abnormalities could also help to account for some of the key
cognitive and behavioural features of these conditions, such as anomalous visual,
motor, attentional, or language processing, as well as some of the associated difficulties
with mood, appetite or digestion, temperature regulation, and sleep (Richardson
and Puri 2000). Reviews of clinical and experimental studies support the idea that
lack of highly unsaturated fatty acids (HUFA) may play a role in these overlapping
developmental conditions (Richardson and Ross 2000). Thus, physical signs of
fatty acid deficiency, such as excessive thirst, frequent urination, rough, dull, or
dry hair and skin, and soft or brittle nails, have been clearly linked with ADHD,
dyslexia, and autistic spectrum disorders, as have reduced blood concentrations
of HUFA and iron (Konofal et al. 2004).
There are relatively few controlled trials to test the effects of fatty acids on
ADHD. One of the first involved evening primrose oil (providing the omega-6
fatty acid, gamma-linolenic acid (GLA)), but this showed little clear benefit (Aman
et al. 1987; Arnold et al. 1989).With the accumulation of evidence that it is the
omega-3 fatty acids that may be washed out in modern diets, emphasis shifted to
fish oils (providing both EPA and DHA), which have been demonstrated to reduce
behavioural and learning difficulties in both ADHD and dyslexia (Burgess 1998;
Richardson and Puri 2002). However, supplementation with pure DHA was twice
found to be ineffective in ADHD (Voigt et al. 2001; Hirayama et al. 2004).A further
pilot randomized study of effects of fatty acids on children with inattention, hyperactivity, and other disruptive behaviours included biochemical analyses that
demonstrated that both the omega-3 fatty acids and vitamin E were correlated
with reductions assessed by the disruptive behaviour disorders (DBD) rating scale.
Vitamin E is commonly added to fish oil as an antioxidant but was not always
declared as an active constituent in earlier studies using EPA and DHA.Thus, the
results of this pilot study suggest the need to declare it as an active ingredient and
for further research with both n-3 fatty acids and vitamin E in children with
behavioural disorders (Stevens et al. 2003). Zinc has been shown to be an effective
adjunct to methylphenidate in treating ADHD at 15 mg/day in a randomized
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study of 44 children (Akhondzadeh et al. 2004). Zinc at 40 mg/day has been shown
to be an effective monotherapy for ADHD in a randomized controlled trial of 400
Turkish children (Bilici et al. 2004). Although this dosage is above physiological
requirements,Turkish children of lower socio-economic status have been shown to
have significantly lowered zinc status (Tanzer et al. 2004).
Linkage of heart and brain function
These findings are consistent with evidence from the treatment of depression and
schizophrenia that EPA, not DHA, may be the key omega-3 fatty acid in functional
disturbances of attention, cognition, or mood.This in itself is surprising as DHA,
not EPA, is found in the brain. One alternative is that EPA may improve brain
blood flow through inhibition of cyclooxygenase and vasoconstrictive eicosanoids
(Ellis et al. 1992). More recently it has been found that the phospholipase
A2–arachidonic acid pathway and 20-hydroxyeicosatetraenoic acid production
may have a regulatory role in cerebral blood flow (Mulligan and MacVicar 2004).
This blood flow carries the brain’s energy supply, which may constitute a limiting
factor to the brain’s information-processing capacity (Peppiatt and Attwell 2004).
Certainly there is a body of literature that suggests that heart function affects brain
function and behaviour; this will be discussed below. It is equally possible that the
therapeutic effects of fatty acids are influenced by the dietary intakes of other
nutrients such as vitamin E (Stevens et al. 2003) or zinc as these nutrients appear to
interact with fatty acid metabolism (Bekaroglu et al. 1996; Wauben et al. 1999).
These data nevertheless suggest that there is a plausible relationship between diet
and a range of developmental conditions with clearly described associated behaviours. More research is required to delineate that relationship. If diet is a protective
factor from these disorders then it can only be hoped that such requirements are
eventually taken into account when assessing standards of dietary adequacy.
Sugar and behaviour
If the amount of energy supplied to the brain puts a limit on its informationprocessing capacity, it might be deduced that high sugar consumption would be
helpful to brain performance.There have been a number of randomized studies
conducted to assess the behavioural and cognitive effects of sugar. An experiment
using a counterbalanced Latin square design involving 48 children, compared the
behavioural effects of sugar, aspartame, and saccharine as a placebo in blind dietary
sequence changes every 3-weeks.The study concluded,‘Even when intake exceeds
typical dietary levels, neither dietary sucrose nor aspartame affects children’s behaviour or cognitive function’ (Wolraich et al. 1994). A study of 48 children may not,
however, be a strong basis on which to form such robust conclusions. Small studies
do not have the numbers for appropriate randomized control for broader extrapolation and may lack the power to detect smaller effects that may be cumulative in the
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population at large. A literature review acknowledged that ‘Sugar clearly does not
induce psychopathology where there was none before, but it may on occasion
aggravate an existing behaviour disorder’ but again the largest study quoted was 76
selected children (Kinsbourne 1994).To further illustrate the complications of dietary
studies, the Wolraich study used vitamin C and riboflavin to assess compliance in
the active cells at dosages comparable to those reported in the literature to improve
cognition and behaviour (e.g. Benton et al. 1995; Heseker et al. 1995). A recent
dose-ranging study of 67 adult students (Flint and Turek 2003) with normal
glucose metabolism suggests that large doses of glucose that increase blood glucose
levels do not influence attention, but that a moderate dose (100 mg/kg) of glucose
selectively impairs measures of impulsivity or disinhibition. Furthermore,
the glycaemic index (broadly how quickly the carbohydrate can be utilized) of
carbohydrate sources also appears to influence cognitive effects in human and
animal studies (Benton et al. 2003). Refining of sugar removes many of
the micronutrients required in carbohydrate metabolism; hence the term empty
calories. It has been argued that the lack of these micronutrients is the reason that
behaviour might be affected by sugar consumption (Schoenthaler 1994). Given
the pervasive use of refined sugar in modern diets and its interactions with health
concerns, there is a strong case for large randomized studies to investigate sugar and
behaviour in more detail.
Mood
While many of us might be ostensibly healthy, we may wonder if taking better care
of our diet would enhance our mood. Researchers have examined the effects of
diet on mood in apparently healthy subjects but, as with other areas reported, the
effects may depend on the dietary baseline, i.e. the quality of the exiting diet. Such
factors may be regional. Intakes of many trace elements are influenced by the soil
types from which the food originates; for example, UK soil is low in selenium.
In a study of 11 healthy men who where fed either a low or a high selenium diet
for 15 weeks, raising selenium intakes beyond the typical US recommended dietary
allowance (RDA) of 70–356 mg had no measured effect on mood but low baseline
erythrocyte selenium correlated with changes in hostile–agreeable and
depressed–elated scales using the profile of mood state (POMS)-B10 assessment
subscales (Hawkes and Hornbostel 1996). The authors concluded that, because
US dietary selenium baselines are higher than in the UK, these findings were consistent with a UK double-blind experimental study (Benton and Cook 1991).
Here 50 subjects significantly decreased ratings of anxiety, depression, and tiredness
over 5 weeks with 100 mg of selenium per day.This was particularly true of those
subjects who had estimated intakes of 28–62 mg per day, while those in the higher
intake ranges of 63–280 mg per day showed less change in mood. It is noteworthy
that the lower range is more typical of UK dietary selenium intakes (MAFF 1997).
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Similarly, low iron status is relatively common and may contribute to lethargy.
Studies of athletes suggest that the lack of energy that results from iron deficiency anaemia can be a serious disincentive to exercise (e.g. Nielson and
Nachtigall 1998). It should be noted that nutritional regimes are routinely
applied with training to enhance athletic excellence. Other factors of the diet
that have been considered in relation to mood are the intakes of carbohydrates.
Benton and Donohoe (1998) assert that carbohydrate intake is associated with
improved mood, while poor mood stimulates the eating of ‘comfort foods’ such
as chocolate. Carbohydrate metabolism predicted results in tests of memory and
cognition in healthy subjects (Donohoe and Benton 2000). The specific mood
response to carbohydrate intake is complex as this has been shown to be influenced by many aspects of the dietary baseline: when food is consumed; the time
delay between meals; the amount consumed; the fibre content; the glycaemic
index of the food; the level of accompanying protein (Benton 2002; Benton et al.
2003).
The relationship between diet and mood has so far not benefited from the
considerable international investment to investigate the relationship between diet
and health. Mood reflects how well we feel in ourselves and hence the quality of
life experienced.This would also be a worthy area to add to the considerations of
dietary adequacy.
Diet and antisocial behaviour
A question remains, however, as to whether diet might affect behaviour to which
we assign free will.This is a common underlying assumption in the criminal justice
system, so this discussion will focus on criminal and antisocial behaviour.
Firstly, let us define what we mean by crime and the broader category of antisocial
behaviour. Central to any form of criminal justice is the notion that culpability can
be attributed. Culpability is distinct from simply establishing guilt as the degree of
individual liability is judged in relation to an action.The classical form of justice
assumes that man is an agent of free will and can choose to commit an offence;
hence culpability can be fully attributed. Crime is judged in relation to a body of
criminal law that sets out offences, that is, acts for which a legal penalty will apply.
Straightforwardly, a crime is deemed to have been committed when one of these
laws is judged to have been broken.When other forms of social rules are judged to
have been broken, such as within an institution, it will be described as antisocial
behaviour.While this serves as a useful distinction, it is recognized that in both
cases it is assumed that the perpetrator would know that such behaviours attract a
sanction, albeit of differing severity.
A dramatic illustration of a possible relationship between diet and behaviour
is the following diet consumed by a persistent criminal offender. He had been
sentenced by UK courts on 13 occasions for stealing trucks in the early hours of
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the morning and on the last three occasions he was imprisoned.This was all he
ever ate.
◆
Breakfast: Nothing (asleep).
◆
Mid-morning: Nothing (asleep).
◆
Lunch time: 4–5 cups of coffee with milk and 2.5 heaped sugars.
◆
Mid-afternoon: 3–4 cups of coffee with milk and 2.5 heaped sugars.
◆
Tea: Fries, egg, ketchup, and 2 slices of white bread; 5 cups of tea or coffee, with
milk and 2.5 heaped sugars.
◆
Evening: 5 cups of tea or coffee, with milk and 2.5 heaped sugars; 20 cigarettes;
£2 worth of sweets, cake, and (if money available) 3–4 pints of beer.
The court was exasperated by his behaviour because on release from prison he
had chosen to steal a truck to return home! Notice that there are no fruits or green
vegetables whatsoever.There are no obvious sources of omega-3 fatty acids.There
are at best modest sources of protein and fibre. Much of the calories come from
sugary drinks and cake. Consider how you might feel if you lived on his diet for
3 months. With the approval of the court he was given dietary education to
improve his eating habits. He eventually trained as a chef. His probation officer
reported that he had not re-offended in 15 years.
Nutritional status of offenders
National dietary surveys have not to date differentiated between offenders and
non-offenders, so the possibility remains that the diets of offenders are somehow
atypical.The most accurate method is to determine this is by assessments of nutritional
status from blood. A study that compared the nutritional status of offenders with
that of non-offending controls found no significant differences in nutritional status.
However, there were differences in sugar metabolism (Gans et al. 1990).This needs
wider population assessments, as such conclusions cannot be taken as typical given
regional variations in diet. It would be a reasonable point to make that there must
be criminals who consume a healthy diet. Perhaps so, but since national dietary
standards were never established with brain function or behaviour in mind, we
really don’t know yet if a diet is adequate from the perspective of the brain.
Reinterpreting crime trends
If nutrition plays a role in our behaviour, then effects from nutrition would not
only have to be in force within individuals but presumably should be capable of
helping shape patterns of social behaviour. In the case of crime, these changes are
considerable over the last century. Using the UK as an example, in 1900 there were
77 934 offences reported which rose to 5 170 843 in 2000, albeit reaching a peak
in 1992, followed by a decline during the 1990s and then a levelling off.
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Total crime in UK by decade
60,000,000
50,000,000
Violence against a person
Total violent crime
Total crime reported
40,000,000
30,000,000
20,000,000
10,000,000
0
1900s
1920s
1940s
1960s
1980s
Fig. 7.1 Total crime in UK
by decade (Data supplied
by National Statistics
Office 2002).
Even when adjusting for population, notifiable offences (broadly more serious)
rose almost 10-fold per person in the UK from the 1950s to the mid-1990s (Home
Office 1997). Rapid changes in reported crime, as illustrated in Fig. 7.1, would
be difficult to explain in terms of genetics for instance.There is no doubting the
relevance of other changes such as socio-economic factors, legislation, and police
practice in these trends. Nevertheless, the scale of change over the decades is considerable.Taking the foregoing into account, a scholarly review of such trends (Rutter
et al. 1998) commented,‘The overall rate of crime has risen severalfold over the last
fifty years, a rise so rapid that it can only be due to some impact in the environment. Clearly if society has been so spectacularly successful in causing the levels of
crime to increase there must be the potential for the right sort of interventions to
be equally effective in causing it to decrease!’
One element of this might be that it is our brain’s environment that is being
impacted. We have after all already considered a range of changes that have
occurred in modern diets.There is evidence that violence is influenced by genetic
susceptibility factors (e.g. Caspi et al. 2002).These effects may themselves be influenced by diet as there is a growing awareness of nutrient-gene interactions. Zinc
for instance has been shown to be involved in the regulation of gene expression
(Dieck et al. 2003; Blanchard et al. 2000) and maintaining the configuration of
mammalian gene transcription proteins (e.g. Hanas et al. 1983;Vallee et al. 1981;
Dieck et al. 2005). In addition, exposure to lead (a nutrient antagonist) correlates
with increased delinquency (Needleman et al. 1996) and this may have increased in
the UK during this period until the introduction of unleaded fuel in the early 1990s
(e.g.Thomson et al. 1989). It has to be recognized, however, that such historical
data have limitations and the connection with changing social patterns going back
many decades is speculative.There is, however, more direct evidence that raises the
possibility that such influences could have increased their grip at a time when
social behaviour has deteriorated.
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Evidence linking diet and antisocial behaviour
A comparison of conventional and nutrition education approaches to rehabilitating
102 offenders over 12 months in the community found that the re-offending rates
(11.9%) of the group given nutrition education were almost a third of that of the
controls (33.8%) receiving conventional probation programmes (Schauss 1978).
An experimental study of 3399 imprisoned juveniles, where refined and sugary foods,
snack foods, and drinks available to the inmates were replaced with unsweetened
fruit juices and popcorn, found that, over a 12-month period, there were 21%
fewer serious antisocial acts, a 25% reduction in assaults, a 100% reduction in suicides,
and a 75% reduction in the use of restraints (Schoenthaler 1983).This study lacked
randomized allocation or placebo control. Schoenthaler subsequently conducted a
placebo-controlled double-blind randomized experimental trial using nutritional
supplements based around the US RDA of minerals and three times the US RDA
of vitamins on 62 13–17-year-old male and female incarcerated juveniles.The active
group committed 28% (15–41%, 95% confidence interval (CI)) fewer rule violations
compared to controls ( p 0.005) (Schoenthaler et al. 1997). It was reported that
this effect was most marked in 16 subjects who had significantly improved their
blood vitamin status during the trial from a low baseline of the following vitamins:
C, thiamin, niacin, pantothenic acid, pyridoxine, and folate. A further randomized
placebo-controlled study of 468 school children aged 6–8 years was conducted
using a food supplement formulation of 50% of the US RDA of vitamins and minerals. Of these children, only 80 had a school discipline record at baseline. It was
reported that antisocial incidents fell significantly ( p 0.02) by 47% (29–65%,
95% CI) for those 40 children on active supplementation who had a discipline
record at baseline (Schoenthaler and Bier 2000).There are more appropriate statistical methods to model these data to deal with the floor effect using a Poisson
regression. However, the broad conclusion that significant improvements in behaviour can also be seen in younger children from a simple dietary adjunct should be
followed up. Hamazaki et al. (1996) found that Japanese university students undertaking exams while receiving supplemental DHA on a randomized double-blind
basis did not show an increase in hostility during a frustration test, while those on
placebo increased hostility.This effect was however, not observed under non-stressful conditions (Hamazaki et al. 1998).A randomized placebo-controlled pilot study
of 30 women with borderline personality disorder found that EPA significantly
reduced ratings of aggression and depression compared to controls (Zanarini and
Frankenburg 2003).While these experimental studies offer broadly encouraging
results, they need to be replicated with larger randomized designs.
With the co-operation of the UK Home Office an empirical study was
conducted to test if poor nutrition is a cause of antisocial behaviour (Gesch et al.
2002).The study was simply designed to provide a powerful test for a general effect
on behaviour, where statistical power was reported as 92% to detect a change in the
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Ratio of rate of disciplinary
incidents supplementation/baseline
1.4
1.2
Active
Placebo
1
0.8
0.6
Error bars drawn at
two standard errors
to indicate the 95%
confidence interval
0.4
0.2
0
Active
Placebo
Before supplementation
1
1
During supplementation
0.737
0.993
Fig. 7.2 Difference between active and placebo groups: intent to treat analysis based on 1132
offences. Test for null hypothesis: Placebo Active.
rate of proven disciplinary offences in a prison. Statistical significance was set at a
conservative 1%. A prison was chosen as all sources of food are known. It was
found that, typically, prisoners did not make appropriate food choices resulting in
many of their dietary intakes falling below UK government dietary standards (Eves
and Gesch 2003). Using a double-blind placebo-controlled randomized stratified
design, 231 young adult prisoners (18–21 years of age) were studied to see whether
nutrient supplementation had any influence on proven disciplinary offences committed by the prisoners.The active nutritional supplements provided broadly the
daily adult requirements of vitamins, minerals, and omega-3 and -6 essential fatty
acids (see Gesch et al. 2002). On an intention to treat basis compared to placebo,
those who received active nutritional supplements committed an average of 26.3%
(8.3–44.33%, 95% CI) fewer offences (p 0.03, two-tailed).This analysis included
everyone recruited to the trial including those who had participated for as little as
3 days but the average was 5 months (see Fig. 7.2).
Having rejected the null hypothesis on an intent to treat basis in a between-groups
comparison, a more sensitive test for the actual effect of treatment (in this analysis,
each individual becomes their own control as we have established that both groups are
matched at baseline by rates of offending) was conducted for the effect on those taking active supplements for a minimum of 2 weeks (n 172;) (see Fig. 7.3).The result
was an average 35.1% reduction of offences (95% CI 16.3–53.9%, p 0.001, twotailed), whereas those taking placebos remained within standard error, proving no
evidence of change.The greatest reduction occurred for the most serious incidents
(including violence) dealt with by governor reports. Based on an analysis of 338 governor reports, the active group committed 37% (11.6–62.4%, 95% CI) fewer governor
reports (p 0.005, two-tailed), whereas the placebo group remained within standard
error (p 0.1, two-tailed) at 10.1% fewer governor reports (16.9–37.1%, 95% CI),
again providing no evidence of change.
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Ratio of rate of disciplinary
incidents supplementation/baseline
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1.4
1.2
Active
Placebo
1
0.8
0.6
Error bars drawn at
two standard errors
to indicate the 95%
confidence interval
0.4
0.2
0
Active
Placebo
Before supplementation
1
1
During supplementation
0.649
0.933
Fig. 7.3 Effect on those treated for more than 2 weeks (N 172). Number of offences 754. Test
for effect: Placebo 1, Active 1.
Thus, with placebos there was no evidence for a reduction in offending over time
spent in the prison, while, in marked contrast, those receiving active nutritional supplements committed significantly fewer disciplinary offences over the same period.
The differences in the rate of offending in the prison could not be explained by
ethnic or social factors, or variations in the administration of governor reports, or
opportunity to offend as they should have been controlled for by the randomized
design: the compliance of both randomly allocated groups was closely matched as
were all baseline measures of behaviour and diet, so it had to be the nutrients in the
capsules that caused the change in behaviour.The issue then is the nutritional quality of the existing dietary baseline.The dietary baseline had been modified (the
independent variable) using nutritional supplements.The supplements were really
an analogue for a better diet but they have the advantage that the nutritional value
is precisely known and allowed for the use of placebo. Ideally, such improvements
in nutritional intake should come from the diet (for a more detailed discussion, see
Eves and Gesch 2003).The dosages provided were physiological rather than high
dose and might be readily achievable with even a modest increase in expenditure
on diet coupled with dietary education.
Given the wide implications, these findings need to be widely replicated.The
participants did not guess accurately what sort of capsules they had been given
either, so the importance of Bryce-Smith’s idea becomes clear; here we have a
potent effect on behaviour that can be measured but not sensed.The findings are
all the more surprising because this age group of prisoners has proved to be notoriously resistant to behavioural improvements (Kershaw 1999). A limitation of the
study was that biochemical measures were not available; they will be required in
any replication to explore the utilization of nutrients and also mediating mechanisms.Thus, having empirically demonstrated an effect on antisocial behaviour, we
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are only at the start of understanding the potential of this intervention. It is quite
possible that, with a better understanding of the range and balance of nutrients
required, the protective effect could be further improved.
Health implications of an adequate diet
It should come as no surprise that ensuring the prisoners’ diets reached UK
government dietary standards did not result in adverse reactions. Indeed, it could be
argued that the real experiment was the ongoing default position where prisoners
were not reaching these dietary standards.The only referral for a possible adverse
event was a young man who was surprised that his evacuations had increased in
frequency from once a fortnight to once every 2 days: the prison doctor rightly
considered this an indicator rather than an adverse event! Here we have criminals
in a maximum-security institution not appreciating what their bodies are telling
them. Some of the participants had not heard of vitamins, let alone knew which
foods contained them; they were not even remotely equipped to make healthy
food choices. Being pragmatic, a combination of supplementation to reinstate
nutrients first coupled with dietary education may be prudent in such populations.
Notwithstanding the seriousness of their crimes, many of them took the trouble to
express gratitude for being involved in the trial.
Implications of a protective effect on behaviour
These findings suggest that diet can affect behaviour to which we assign free will. Indeed, it
is difficult to see how free will could be exercised without involving brain function. Furthermore, these effects may be far more potent than we realized. This
raises the question as to what life would have held for these 231 young men if
they had grown up with better nourishment.The only studies so far published that
provide any indication are longitudinal studies conducted in Mauritius.An experimental enrichment programme, comprising nutrition, education, and physical
exercise for 83 children aged 3 to 5 years, yielded significantly lower scores for
schizotypal personality and antisocial behaviour at age 17 years and for criminal
behaviour at age 23 years compared with 355 matched controls (Raine et al. 2003).
The beneficial effects of the intervention were greatest for children who showed
signs of malnutrition at 3 years of age.A second birth cohort of 1795 were assessed
for signs of malnutrition at age 3 years. Cognitive measures were assessed at ages 3
and 11 years, while antisocial, aggressive, and hyperactive behaviour was assessed
at ages 8, 11, and 17 years.The authors concluded that there was a dose-response
relationship between the degree of malnutrition and degree of externalizing
behaviour at ages 8 and 17 (Liu et al. 2004).They argue that these findings suggest
that reducing early malnutrition may help reduce later antisocial and aggressive
behaviour. Given the implications, this needs to be replicated. It may be simplistic,
but if there are fewer crimes committed there will also be fewer victims.
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Observational evidence
The experimental studies above are supported by observational studies that indicate
relationships between antisocial behaviour and a number of nutrients but it is
recognized that these relationships will require more research to delineate.
Violent offenders were found to have lowered levels of omega-3 and omega-6 but
raised omega-9 essential fatty acids compared to age-matched non-offending
controls (Corrigan et al. 1994). A cross-national epidemiological analysis found a
significant inverse correlation between seafood consumption and incidence of
homicides (Hibbeln 2001). Hibbeln et al. (1998) found an inverse relationship
between omega-3 plasma essential fatty acids and levels of the metabolites of serotonin
and dopamine taken from cerebrospinal fluid in violent offenders, but this was
not found with non-offending controls. Stevens et al. (1996) found an increased
number of behavioural problems in 6–12-year-old boys with lower plasma concentrations of omega-3 fatty acids.Virkkunen et al. (1987) reported abnormalities
in plasma phospholipid concentrations of fatty acids in offenders with a history of
alcohol abuse.Violent offenders were found to have significantly lower cholesterol
levels than non-violent subjects who were matched by age, sex, alcohol indices,
and education (Golomb et al. 2000).Walsh et al. (1997) reported significantly elevated copper/zinc ratios in assaultive young males compared to non-assaultive controls. Plasma homocysteine has been positively associated with ratings of hostility
and anger (Stoney and Engebretson 2000). Regulation of homocysteine is
dependent on folate, cobalamin (vitamin B 12 ), and pyridoxine (vitamin B 6 ).
Depressed patients, for instance, were found to have raised homocysteine levels
and lowered cobalamin and folate (Bottiglieri et al. 2001).There may also be a case
for addressing individual dietary requirements. A review of 207 subjects selected
from 258 consecutive cases suggested that self-reports of violence were significantly reduced compared to baseline by individualized nutritional therapy. Such
data are difficult to interpret without controls but the authors appropriately
argued for the need to follow up with randomized trials to test efficacy (Walsh
et al. 2004).
There may even be behavioural implications for trace elements not yet accepted
as essential for human health.A study found significantly fewer homicides, suicides,
and rapes in counties of Texas with naturally occurring levels of lithium in drinking water in the range 70–170 g/L compared to rates in those counties with little
or no lithium; these dosages are far lower than those used in medicine. Similarly,
violent offenders were found to have less lithium in their scalp hair than controls.
These studies simply demonstrate correlations but a double-blind randomized trial
of 24 former drug addicts supplemented with 400 g lithium for a month found
significant improvements in mood, reflecting changes in happiness, friendliness, and
energy. The author argued a case for the essentiality of lithium in humans at
dosages of 1000 g a day (Schrauzer 2002).
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Physiological markers
Physiological markers linked to nutrition also seem to be predictive of antisocial
behaviour (Christensen et al. 1996). It has already been reported that the output of
the heart supplies the brain with energy, the amount of which may be the limiting
factor on information-processing, and one might presume has an impact on behaviour.This appears to be so. Low heart rate variability is thought to be a sensitive
marker of low autonomic nervous system function (Akselrod and Gordon 1985) and
is considered to measure autonomic adaptation; as such it is considered representative
of more basic brain functioning.Wadsworth (1976) reported a stronger correlation
between delinquency and lowered resting pulse rate than between delinquency
and social deprivation. Children aged 6–7 years with mental health symptoms
could be distinguished from controls by low reactivity in parasympathetic and
sympathetic systems (Boyce et al. 2001). In a 15-year longitudinal study of the
siblings of juvenile delinquents, abnormalities in autonomic function identified at
age 15 years predicted with 75% accuracy which subjects would be incarcerated
by the age of 29 (Raine et al. 1995). Low heart rate variability also predicted
psychopathology and hostility in a 2-year longitudinal analysis of urban boys at risk
of delinquency (Pine et al. 1998). Similarly, heightened autonomic nervous system
responsiveness was associated with a reduced likelihood of criminal convictions in
subjects at social high risk for criminal behaviour (Brennan et al. 1997).
Physiological mechanisms
The research suggests that nutrition influences behaviour, but the mechanisms by
which this occurs are not fully understood. It is, however, widely accepted that
antisocial behaviours are influenced by the regulation of serotonin (e.g. Linnoila
et al. 1983; Stanley et al. 2000;Virkkunen et al. 1995), so this will be used as an illustration. Serotonin is derived from the dietary amino acid tryptophan.To demonstrate
that dietary tryptophan depletion results in increased aggressive responses,
researchers had to control for other possible explanations such as food depletion
causing an increase in aggression (Bjork et al. 1999).This illustrates that nutrients
tend to interact with many mechanisms operating in parallel (see also Stacey et al.
1994). Providing piglets with supplemental AA and DHA (the two fatty acids considered so influential in our brain development) significantly increased concentrations of serotonin, tryptophan, and dopamine in the frontal cortex of their brains
(de la Presa Owens and Innis 1999).Vitamin E deficient diets have been shown in
animal studies to lower serotonin in rat striatum (Castano et al. 1993). Zinc is known
to modulate the function of a number of neurotransmitter gated ion channels,
including recombinant murine 5-hydroxytryptamine (3A) (5-HT(3A)) receptors,
and it potentiates serotonin-induced responses (Hubbard and Lummis 2000).
Furthermore, animal studies have shown that low iron and zinc intakes predispose
towards aggression (Halas and Reynolds 1977; Munro 1987). Pyridoxine has
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been demonstrated in monkey brains to have a regulatory effect on the conversion
of 5-hydroxy-L-trytophan (5-HTTP), a precursor of serotonin (Hartvig et al. 1995).
Oral doses of pyridoxine were found to influence blood serotonin and pyridoxal
phosphate levels in hyperactive patients (Bhagavan et al. 1975). It is not suggested
that these studies offer proof of mechanisms that are at work in antisocial behaviour, as this will require a great deal more research, but they do illustrate the potential for plausible physical pathways to be identified by which levels of nutrients
could affect levels of antisocial behaviour.
Mediation of dietary effects on antisocial behaviour
How such effects are mediated is another important question.The picture is far
from clear at this stage but inhibitory mechanisms are considered fundamental
components of the attentional and higher cognitive processes that form the key
dysfunctions of ADHD, for example, which is a common precursor of antisocial
personality disorder (ASP; e.g.Taylor 1998; Rubia et al. 1998). Impulse control is
a current focus of interest for how nutrients might impact behaviour. Adults with
ASP, conduct disorder, and aggressive impulsiveness have been shown to have
neuropsychological deficits in frontal-lobe-mediated paradigms (Pennington and
Bennetto 1993; Brower and Price 2001). Moreover, low executive functioning has
been shown to correlate with measures of physically aggressive behaviour (Giancola
et al. 1998; Foster et al. 1993; LaPierre et al. 1995).Violent offenders have also been
found to be deficient in shifting attention from one category to another when
compared to normal control subjects (Bergvall et al. 2001). Poor development of
self-directedness and cooperative traits in forensic populations may be associated
with deficits in neuropsychological functioning (Bergvall et al. 2003).
Replication
Large (N 700) clinical trials are planned within the UK and Dutch prison
systems to investigate the relationship between a participant’s nutritional status
(measured from blood samples) and changes in specific nutrient groups with the
following outcomes, antisocial behaviours, violence, drug abuse, self-harm, impulse
control, attention, planning, interpersonal relating, and food choice, with concomitant implications for reassessing dietary standards and our understanding of such
behaviours in the community.
Integrating nutrition with existing risk factors for antisocial
behaviour
There do appear to be interactions between our social and physical environment as
Bryce-Smith (1986) predicted.While this may seem daunting initially, there are
many positive aspects to this, as diet could provide an additional means to promote
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behavioural well-being at a time when criminal justice resources are under stress.
These findings also may improve our understanding of established socio-economic
risk factors such as low income, family interactions, and peer-groups that correlate
with offending (Blackburn 2002).There will also always be a biophysical component to any social situation, as we all need to eat.This will interact with both individual and environmental theories of crime (Blackburn 2002).There is a great deal
of research into ‘risk factors’ that affect the behaviour of juveniles (Smith 1995;
Rutter et al. 1998) including, for example, the breakdown of families (Heiss 1995).
However, one of the social functions of families is to provide food, so it would be
illuminating to investigate the extent to which diets interact with such breakdowns. It is well established that diet is related to income (e.g.WHO 2003). If we
no longer produce our own food, the costs per calorie of healthy foods like fruits
and green leafy vegetables are typically much higher because they contain so few
calories.The healthy energy-dense foods like lean meats and fish are much more
expensive than more highly refined energy-dense foods derived from saturated fats,
white flour, and refined sugars.These cheap, energy-dense foods are likely to seem
more attractive and affordable if you have a limited income.Those on low incomes
are likely to face the dual pressures of socio-economic and physiological stress as a
consequence of not easily affording adequate diets.The cycle is therefore self-reinforcing. If we grow up with friends in this environment, this may conceivably
increase the wayward influence of peer pressure as the behaviour of our friends is
more likely to be undermined by poor nutrition.We will presumably also be subject to the vagaries of a poor social environment. However, this would not explain
why, in general, more boys get into trouble than girls and this reaches a peak in late
adolescence. One might wonder how diet could be involved in these trends.The
link is speculative at this stage but, for instance, differences have been found in
DHA metabolism between males and females (Burdge and Wootton 2002; Burdge
et al. 2003). A factor in the peak age of offending may turn out be the more pronounced growth spurt in young males, which brings with it a range of physiological changes such as rapid growth that may place the brain under increased
nutritional stress (Gesch 2002). If this scenario is correct, it highlights the importance of providing healthy meals to schoolchildren to help break this self-reinforcing cycle. The British Government recently concluded that just 6% of
schoolchildren made healthy food choices at school meals and, according to the
Times Educational Supplement, 14 April 2004, ‘The Government has been forced
to pump £342 million into school behaviour improvement programmes.’ In view
of the foregoing, these two facts may not be coincidence.Would it not be prudent
to apply the precautionary principle and to try our best to ensure that all our
children at least reach existing dietary standards? Large studies of the effects of diet
in schools are being planned.
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Implications in criminal justice
It is not suggested that nutrition is the only explanation of antisocial behaviour,
only that it might form a significant part. Unlike in medicine, however, most of the
‘risk factors’ targeted in criminal justice interventions are typically correlations,
which leaves questions of volition, culpability, prevention, and rehabilitation open
if cause and effect are not formally demonstrated with appropriate randomized
experimental designs.This leaves crucial questions unanswered.What causes someone to commit a crime or behave in an antisocial manner when others do not?
How do you predict or prevent offending unless you know what causes it? How
do you accurately focus resources unless you know about causes? For instance, the
public costs of testing cognitive skills approaches in English prisons was reported in
the London Times (18 November 2003) to cost £150 000 000 and this approach
was found to be ineffective (Cann et al. 2003). In contrast, The Economist of 29 June
2002 reported the cost of the nutritional approach to be as little as 0.2% of that
expended on custody. Faced with escalating costs, there is a climate of increasing
honesty in the US that federal criminal justice policies are not underpinned by
rigorous evidence, with statements such as ‘The effectiveness of most crime prevention strategies will remain unknown until the nation invests more in evaluating
them’ (Sherman et al. 1997),‘It’s easy to fool yourselves about efficacy if you haven’t
done a proper clinical trial’ (Marshall 2000), and ‘Progress is often thwarted by
Government programmes and strategies that are not based on rigorous evidence’
(Baron et al. 2003). The report by the US Department for Justice and Collation for
Evidence-Based Policy (Baron et al. 2003) recommended that in future interventions should be evaluated by randomized designs as the sole basis for strong evidence of efficacy with which to underpin criminal justice policy. Evidence is, after
all, only as good as the means used to obtain it! Ironically, the finding that a better
diet can positively impact on behaviour exceeds the standards suggested as a strong
basis of evidence to underpin criminal justice strategy but this approach is not yet
assimilated into criminal justice thinking. These studies will need to be widely
replicated and, if so, we may have finally demonstrated a causal factor in antisocial
behaviour. Further studies are also planned in the UK to test effects of nutrition on
crime in the community. If the finding that diet can positively influence behaviour
directly is widely replicated, it questions the underlying assumptions of the classical
form of justice where it is assumed that behaviour is entirely a matter of free will.
The picture will then be more complex but the solution perhaps more straightforward. Some of these factors will act in ways that we can see and some of them will
not, so we will need a broader interpretation of the causes of antisocial behaviour in
criminal justice, where physical and social functioning are both considered relevant
to culpability.
Awareness offers hope because, if this scenario is correct, this process can be reversed
if we choose to nourish our children rather than condemn them for influences on
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their behaviour that we have not taken into account. In doing so we may need to
choose if we prefer to lock up ever more of our nation’s children or to nourish
them properly. Indeed, one of the difficulties in criminal justice is knowing when to
intervene. Pre-emptive involvement in the criminal justice system runs the risk of
being prejudicial to those who might not offend and has been shown to accelerate
criminal careers through association, while intervening too late can also result in
escalation. In marked contrast, how is providing a healthy diet going to be prejudicial at any stage? The Dutch Ministry of Justice is actively investigating this approach
and made a telling comment: ‘There are only positive side-effects to providing
offenders with a better diet!’
According to a UK Home Office report (Brand and Price 2000),‘The total cost
of crime to England and Wales in 1999/2000 is estimated at around £60 billion,
although this figure is still far from comprehensive, as it does not include important
costs such as fear of crime or quality of life impacts.’ If diet could achieve even a
modest impact on these costs the benefits could be vast.There is strong case to
conduct further large randomized trials to explore if diet can reduce crime in the
community and antisocial behaviours in prisons and other institutions such as
schools.
Discussion
The global implications for well-being
A range of evidence has been reviewed that suggests that the dietary requirements
for good health are also supportive of positive social behaviour.These findings need
to be widely replicated, as potentially there are global implications.The interventions that have been reviewed simply provide nutrients at physiological dosages
that are already known to be essential for health. Providing a healthy diet does
absolutely no harm, yet we have arrived at a situation where many of the human
population do not obtain even this. Millions starve while millions suffer from
diseases of excess and yet we spend untold amounts on medical treatment to treat
illness and prisons to curb behaviour. What if much of this suffering could be
prevented?
Good nutrition is essential irrespective of race, age, legislative boundaries, if you
are in prison, or in a rich or developing country.This is a basic need that unites
us all: hence it is not where you eat that is important but what you eat. Humans
are, after all, both social and physical beings—the hardware and software of life, so
to speak. Nutrition can impact on both aspects and thus spans both nature and
nurture. How we interact with food is likely to be a complex function of choice,
family, peer-group, physical activity, economics, food distribution, and physiology.
Food plays an important role in our social structures. Much of traditional family
routine is based around meals. A mother’s love, courtship, and friendship are often
expressed through giving food. We incorporate food into medicine and our
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religious practices such as offerings to deities or sacrament.Yet for every social
situation there will always be a biophysical analogy. Irrespective of what we eat,
getting food into one’s mouth will be socially mediated but one’s mouth is the
gateway to the physical world. Crucially, our physiological responses to our diet
are likely to be the most finite component of this equation, as they seem to be
primarily derived from our evolution.This may explain why longitudinal studies
can link a child’s diet (or, for instance, childhood exposure to lead) with crime as
an adult.This is not a reinterpretation of crude determinism because this is a feedback cycle where choice will inform what we put into our mouths, while the
nutrients in the food will support the operation of the senses that inform our
choice (for instance the retina is 30% AA and DHA). It is worth reiterating that
some of these factors will act in ways that we can see and some of them will not,
so we need a broader interpretation of what promotes well-being, where physical
and social functioning are both considered relevant.The brain needs to be nourished in two ways: love, nurturing, education as well as the nutrients for the brain
to function properly. Not one, not the other, but both. That applies to both the
rich and poor nations.
If we really are what we eat then changing our diet will change us.
We seem to have made major changes to modern diets in a relatively short space
of time with little or no systematic examination for potential impacts on brain
function or behaviour. Hence, evidence of such impact is only emerging on a
retrospective basis. More should be done to prospectively assess such impact.This
not only relates to the food industries. Such a basic issue also seems to have passed
largely unnoticed between the boundaries of academic disciplines and the authorities that construct dietary standards. There is a need for contiguous scientific
disciplines to cooperate to investigate the broader picture. Because nutrition is
fundamental for life and also the composition of our brains, its effects are likely to
be pervasive.The health consequences of modern diets are already visible but we
are only beginning to appreciate them in brain chemistry, mental health, cognition,
and behaviour.We are likely to interpret behavioural problems in terms of what we
can see, so it is feasible that, on a societal scale, the effects of poor diet are liable to
be greatly amplified, as greater numbers of social interactions are subject to these
hitherto unnoticed influences on our behaviour. These effects may even shift
the socially acceptable norms of behaviour without our knowledge. It may sound
far-fetched but few would have predicted the potency of effect shown in the
prison study.There is even research being planned to explore the role of nutrition
in artistic expression. Physiological factors like nutrition may also turn out to be
important in understanding the tragic and irrational acts that litter news broadcasts
and seem to defy a rational explanation. They may add to, rather than supplant
existing explanations. Compared to the myriad of socio-economic problems found
in deprived areas, nutrition may actually be one of the more straightforward factors
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to change. An intriguing aspect of our British prison study is that the prisoners
received three meals a day and, despite making poor food choices, their diets were
possibly better than those consumed by many young men of the same age in the
community.Yet the improvement in behaviour from boosting their diets was highly
significant.We do not know if the improvement in behaviour would have come
from raising the prisoners to existing dietary standards or because some would have
exceeded them slightly.We have limited knowledge of what the optimum ranges
of nutrients are from a behavioural perspective because dietary standards have not
really considered this. The bottom line here is that dietary standards need to be
reassessed to take into account mental health, behavioural, developmental, and
cognitive parameters. It is recognized that this will be a major undertaking involving
extensive research. However, an implication is that, for a great number of people,
their ability to behave sociably could be improved by what they eat, without them
even being aware of it. It is hard to imagine anything that might impact on the
future well-being of our species so directly.
Research is emerging that suggests that good nutrition is potentially inexpensive, humane, and effective at promoting health as well as social behaviour. Most
importantly, people’s positive potential might be realized if such an approach is
taken at a time when global resources are under stress. To make an analogy,
no amount of energy spent on software will resolve a hardware problem. Nature
offers us a clue about the way forward by providing natural foodstuffs that grow
in harmony with their environment and invariably contain a range of nutrients
in dosages to which our metabolism is attuned. It should come as no surprise,
therefore, that many vitamins, minerals, and essential fatty acids seem to promote
aspects of well-being whether it be health or behaviour—particularly those
nutrients that modern dietary practices have rendered less available. If nutrition
was truly seminal in raising our ancestors to a new level of functioning, then
let us rethink our present-day attitude to food. We need to develop our understanding of the dosage and range of nutrients required to positively impact on
the human condition. It may be a recipe that goes beyond individual well-being;
it may be a recipe for peace.
Acknowledgements
Bernard is honoured to work as part of a broad multidisciplinary collaboration
comprising of many eminent academic colleagues as well as the distinguished
trustees of Natural Justice, all of whom have contributed with wisdom and
generosity. The work is therefore a synthesis of these important contributions.
Bernard would particularly like to thank Professor Michael Crawford, Dr Sean
Hammond, Professor Malcolm Peet, Dr Alex Richardson, and Professor John Stein
for their kind contributions to the text.
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References
Aboderin, I., et al. (2001). Life course perspectives on coronary heart disease, stroke and diabetes: key issues
and implications for policy and research.World Health Organization, Geneva.
Acar, N., Chardigny, J.M., Berdeaux, O., Almanza, S., and Sebedio, J.L. (2002). Modification
of the monoaminergic neurotransmitters in frontal cortex and hippocampus by dietary trans
alpha-linolenic acid in piglets. Neurosci. Lett. 331 (3), 198–202.
Akhondzadeh, S., Mohammadi, M.R., and Khademi, M. (2004). Zinc sulfate as an adjunct to
methylphenidate for the treatment of attention deficit hyperactivity disorder in children:
a double blind and randomized trial. BMC Psychiatry 4 (1), 9.
Akselrod, S. and Gordon, D. (1985) Hemodynamic regulation: investigation by spectral analysis.
Am. J. Physiol. 249, 867–75.
Aman, M.G., Mitchell, E.A., and Turbott, S.H. (1987).The effects of essential fatty acid
supplementation by Efamol in hyperactive children. J. Abnorm. Child Psychol. 15 (1), 75–90.
Angel, J.L. (1984). Health as a crucial factor in the changes from hunting to developed farming
in the eastern Mediterranean. In Paleopathology at the origins of agriculture (ed. M.N. Cohen and
G.J. Armelagos), pp. 51–74. Academic Press, New York.
Arnold, L.E., Kleykamp, D.,Votolato, N.A., Taylor, W.A., Kontras, S.B., and Tobin, K. (1989).
Gamma-linolenic acid for attention-deficit hyperactivity disorder: placebo-controlled
comparison to D-amphetamine. Biol. Psychiatry 25 (2), 222–8.
Astrup, A., et al. (2000).The role of low-fat diets in body weight control: a meta-analysis of ad
libitum dietary intervention studies. Int. J. Obesity 24, 1545–52.
Ayala, S. and Brenner, R.R. (1983). Essential fatty acid status in zinc deficiency. Effect on lipid
and fatty acid composition, desaturation activity and structure of microsomal membranes of
rat liver and testes. Acta Physiol. Lat. Am. 33 (3), 193–204.
Ayala, S. and Brenner, R.R. (1987). Effect of zinc deficiency on the in vivo biosynthesis of fatty
acids of the linoleic series in the rat. Acta Physiol. Pharmacol. Latinoam. 37 (3), 321–30.
Barker, D.J.P. (1995). Fetal origins of coronary heart disease. Br. Med. J. 311, 171–4.
Barker, D.J.P., Osmond, C., Winter, P.D., Margetts, B., and Simmonds, S.J. (1989).Weight in
infancy and death from ischaemic heart disease. Lancet 2, 577–80.
Barker, D.J.P., Forsén, T., Uutela, A., Osmond, C., and Eriksson, J.G. (2001). Size at birth and
resilience to the effects of poor living conditions in adult life: longitudinal study. Br. Med. J. 323,
1273–6.
Baron, J., et al. (2003). Bringing evidence based progress to crime and substance-abuse policy: a
recommended federal strategy. Coalition for Evidence-based Policy, sponsored by the Council for
Excellence in Government,Washington, DC.
Bekaroglu, M., et al. (1996). Relationships between serum free fatty acids and zinc, and attention
deficit hyperactivity disorder J. Child Psychol. Psychiatry 37, 225–7.
Bennis-Taleb, N., Remacle, C., Hoet, J.J., and Reusens, B. (1999). A low-protein isocaloric
diet during gestation affects brain development and alters permanently cerebral cortex blood
vessels in rat offspring. J. Nutr. 129, 1613–19.
Benton, D. (2001). Micro-nutrient supplementation and the intelligence of children. Neurosci.
Biobehav. Rev. 25, 297–309.
Benton, D. (2002). Carbohydrate ingestion, blood glucose and mood. Neurosci. Biobehav. Rev.
26 (3), 293–308.
Benton, D. and Cook, R. (1991). Selenium supplementation improves mood in a double-blind
crossover trial. Biol. Psychiatry 29, 1092–8.
30/9/05
12:27 PM
Page 203
Benton, D. and Donohoe, R.T. (1999).The effects of nutrients on mood. Public Health Nutr.
2 (3a), 403–9.
Benton, D., Haller, J., and Fordy, J. (1995).Vitamin supplementation for 1 year improves mood.
Neuropsychobiology 32 (2), 98–105.
Benton, D., Ruffin, M.P., Lassel, T., Nabb, S., Messaoudi, M.,Vinoy, S., Desor, D., and Lang,V.
(2003).The delivery rate of dietary carbohydrates affects cognitive performance in both rats
and humans. Psychopharmacology (Berl.) 166 (1), 86–90.
Bergvall, A., Wessely, H., Forsman, A., and Hansen, S. (2001). A deficit in attentional
set-shifting of violent offenders. Psychol. Med. 31 (6), 1095–105.
Bergvall, A.H., Nilsson, T., and Hansen, S. (2003). Exploring the link between character,
personality disorder, and neuropsychological function. Eur. Psychiatry 18 (7), 334–44.
Bhagavan, H.N., Coleman, M., and Coursin, D.B. (1975).The effect of pyridoxine
hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children.
Pediatrics 55 (3), 437–41.
Bilici, M.,Yildirim, F., Kandil, S., Bekaroglu, M.,Yildirmis, S., Deger, O., Ulgen, M.,
Yildiran, A., and Aksu, H. (2004). Double-blind, placebo-controlled study of zinc sulfate in
the treatment of attention deficit hyperactivity disorder. Prog. Neuropsychopharmacol. Biol.
Psychiatry 28 (1), 181–90.
Bjork, J.M., Dougherty, D.M., Moeller, F.G., et al. (1999).The effects of tryptophan depletion
and loading on laboratory aggression in men: time course and a food-restricted control.
Psychopharmacology 142, 24–30.
Blackburn, R. (2002). The psychology of criminal conduct: theory, research and practice.Wiley and Sons,
Chichester.
Blanchard, R.K. and Cousins, R.J. (2000). Regulation of intestinal gene expression by dietary
zinc: induction of uroguanylin mRNA by zinc deficiency. J. Nutr. 130, 1393S–1398S.
Blumenschine, R.J. (1991). Hominid carnivory and foraging strategies, and the socio-economic
function of early archaeological sites. Phil.Trans. R. Soc. Lond. B 334, 211–21.
Bottiglieri, T., Laundy, M., Crellin, R., Toone, B.K., Carney, M.W., and Reynolds, E.H.
(2001). Homocysteine, folate, methylation and monoamine metabolism in depression. J. Neurol.
Neurosurg. Psychiatry 70 (3), 419.
Boyce, W.T., Quas, J., et al.: MacArthur Assessment Battery Working Group of the MacArthur
Foundation Research Network on Psychopathology and Development (2001). Autonomic
reactivity and psychopathology in middle childhood. Br. J. Psychiatry 179, 144–50.
Brand, S. and Price, R. (2000). The economic and social costs of crime, Home Office Research study
217. Home Office, London.
Brennan, P., Raine, A., Schulsinger, F., Kirkegaard-Sorensen, L., Knop, J., Hutchings, B.,
Rosenberg, R., and Mednick, S. (1997). Psychophysiological protective factors for male
subjects at high risk for criminal behavior. Am. J. Psychiatry 154, 853–5.
Brettingham, M. (2004). Depression and obesity are major causes of maternal death in Britain.
Br. Med. J. 329, 1205.
Briefel, R.R., Biolostosky, K., Kennedy-Stevenson, J., et al. (2000). Zinc intake of the US
population: findings from the Third National Health and Nutrition Examination Surveys
1988–1994. J. Nutr. 130, 1367–73.
Broadhurst, C.L., Wang,Y., Crawford, M.A., Cunnane, S.C., Parkington, J.E., and Schmidt, W.F.
(2002). Brain-specific lipids from marine, lacustrine, or terrestrial food resources: potential
impact on early African Homo sapiens. Comp. Biochem. Physiol. B Biochem. Mol. Biol. 131 (4),
653–73.
203
204
30/9/05
12:27 PM
Page 204
BERNARD GESCH
Brower, M.C. and Price, B.H. (2001). Neuropsychiatry of frontal lobe dysfunction in violent
and criminal behaviour: a critical review. J. Neurol. Neurosurg. Psychiatry 71, 720–6.
Bryce-Smith, D. (1986). Environmental chemical influences on behaviour, personality, and
mentation, Royal Society of Chemistry John Jeyes Lecture. Int. J. Biosoc. Res. 8 (2), 115–50.
Bryce-Smith, D. and Simpson, R.I. (1984). Case of anorexia nervosa responding to zinc
sulphate. Lancet 2 (8398), 350.
Burdge, G.C. and Wootton, S.A. (2002). Conversion of alpha-linolenic acid to eicosapentaenoic,
docosapentaenoic and docosahexaenoic acids in young women. Br. J. Nutr. 88 (4), 411–20.
Burdge, G.C., Delange, E., Dubois, L., Dunn, R.L., Hanson, M.A., Jackson, A.A., and
Calder, P.C. (2003). Effect of reduced maternal protein intake in pregnancy in the rat on the
fatty acid composition of brain, liver, plasma, heart and lung phospholipids of the offspring
after weaning. Br. J. Nutr. 90 (2), 345–52.
Burgess, J.R. (1998). Attention deficit hyperactivity disorder: observational and interventional
studies. In NIH workshop on omega-3 essential fatty acids and psychiatric disorders, September 2–3,
1998. National Institutes of Health, Bethesda, Maryland.
Cann, J., Falshaw, L., Nugent, F., and Friendship, C. (2003). Understanding what works: accredited
cognitive skills programmes for adult men and young offenders, Home Office findings 226. Home
Office, London.
Carney, R.M., Saunders, R.D., et al. (1995). Association of depression with reduced heart rate
variability in coronary artery disease. Am. J. Cardiol. 76, 562–4.
Caspi, A., McClay, J., Moffitt, T.E., Mill, J., Martin, J., Craig, I.W., Taylor, A., and Poulton, R.
(2002). Role of genotype in the cycle of violence in maltreated children. Science 297 (5582),
851–4.
Castano, A., Herrera, A.J., Cano, J., and Machado, A. (1993). Effects of a short period of
vitamin E-deficient diet in the turnover of different neurotransmitters in substantia nigra and
striatum of the rat. Neuroscience 53 (1), 179–85.
CDC (Centers for Disease Control) (2002).Youth risk behaviour surveillance. Morb. Mortal.Wkly
Rep. 51 (SS04), 1–64.
Christensen, J.H., Gustenhoff, P., et al. (1996). Effect of fish oil on heart rate variability in survivors
of myocardial infarction: a double blind randomized controlled trial. Br. Med. J. 312, 677–8.
Christensen, J.H., Korup, E., et al. (1997). Fish consumption, n-3 fatty acids in cell membranes,
and heart rate variability in survivors of myocardial infarction with left ventricular dysfunction.
Am. J. Cardiol. 79, 1670–3.
Christensen, J.H., Christensen, M.S., et al. (1999). Heart rate variability and fatty acid content of
blood cell membranes: a dose–response study with n-3 fatty acids. Am. J. Clin. Nutr. 70, 331–7.
Clover, C. (2004). The end of the line: how over-fishing is changing the world and what we eat. Ebury
Press, London.
Colantuoni, C., Schwenker, J., McCarthy, J., Rada, P., Ladenheim, B., Cadet, J.L.,
Schwartz, G.J., Moran, T.H., and Hoebel, B.G. (2001). Excessive sugar intake alters
binding to dopamine and mu-opioid receptors in the brain. Neuroreport 12 (16), 3549–52.
Colantuoni, C., Rada, P., McCarthy, J., Patten, C., Avena, N.M., Chadeayne, A., and
Hoebel, B.G. (2002). Evidence that intermittent, excessive sugar intake causes
endogenous opioid dependence. Obesity Res. 10 (6), 478–88.
Cordain, L., Miller, J.B., Eaton, S.B., and Mann, N. (2000). Macronutrient estimations in
hunter–gatherer diets. Am. J. Clin. Nutr. 72 (6), 1589–92.
Corrigan, F.M., Gray, R., Strathdee, A., et al. (1994). Fatty acid analysis of blood from violent
offenders. J. Forens. Psychiatry 5 (1), 83–92.
30/9/05
12:27 PM
Page 205
Crawford, M.A. (1968). Fatty-acid ratios in free-living and domestic animals. Possible implications
for atheroma. Lancet. 22:1(7556), 1329–33.
Crawford, M.A. and Sinclair, A.J. (1972). Nutritional influences in the evolution of the
mammalian brain. In Lipids, malnutrition and the developing brain, A Ciba Foundation Symposium
19–21 October 1971 (ed. K. Elliot and J. Knight), pp. 267–92. Elsevier, Amsterdam.
Crawford, M.A., Casperd, N.M., and Sinclair, A.J. (1976).The long chain metabolites of
linoleic acid and linolenic acids in liver and brain in herbivores and carnivores. Comp. Biochem.
Physiol. B 54 (3), 395–401.
Crawford, M.A., Bloom, M., Broadhurst, C.L., Schmidt, W.F., Cunnane, S.C., Galli, C.,
Gehbremeskel, K., Linseisen, F., Lloyd-Smith, J., and Parkington, J. (1999). Evidence for
the unique function of docosahexaenoic acid during the evolution of the modern hominid
brain. Lipids 34 (Suppl.), 39–47.
Cunnane, S.C., Francescutti,V., Brenna, J.T., and Crawford, M.A. (2000). Breast-fed infants
achieve a higher rate of brain and whole body docosahexaenoate accumulation than formula
fed infants not consuming dietary docosahexaenoate. Lipids 35, 105–11.
Curl, C.L., Fenske, R.A., Elgethun, K. (2003). Organophosphorus pesticide exposure of urban
and suburban preschool children with organic and conventional diets. Environ. Health Perspect.
111 (3), 377–82.
Cutler, J.A., Follmann, D., and Allender, P.S. (1997). Randomized trials of sodium reduction:
an overview. Am. J. Clin. Nutr. 65, 643–51.
Davis, K.L., Kahn, R.S., Ko, G., and Davidson, M. (1991). Dopamine in schizophrenia:
a review and reconceptualization. Am. J. Psychiatry 148 (11), 1474–86.
de la Presa Owens, S. and Innis, S.M. (1999). Docosahexaenoic and arachidonic acid prevent
a decrease in dopaminergic and serotoninergic neurotransmitters in frontal cortex caused by
a linoleic and alpha-linolenic acid deficient diet in formula-fed piglets. J. Nutr. 129, 2088–93.
de Onis, M. and Blössner, M. (2000). Prevalence and trends of overweight among preschool
children in developing countries. Am. J. Clin. Nutr. 72, 1032–9.
de Onis, M., Blössner, M., and Villar, J. (1998). Levels and patterns of intrauterine growth
retardation in developing countries. Eur. J. Clin. Nutr. 52, S5–S15.
DePetrillo, P., Speers, d’A.E., and Ruttimann, U. (1999). Determining the Hurst exponent of fractal
time series and its application to electrocardiographic analysis. Comput. Biol. Med. 29, 393–406.
Dieck, H., Doring, F., Roth, H.P., and Daniel, H. (2003). Changes in rat hepatic gene
expression in response to zinc deficiency as assessed by DNA arrays. J. Nutr. 133, 1004–10.
Dieck, H., Doring, F., Fuchs, D., Roth, H.P., and Daniel, H. (2005).Transcriptome and proteome
analysis identifies the pathways that increase hepatic lipid accumulation in zinc-deficient rats.
J. Nutr. 135(2), 199–205.
Doll, R. and Peto, R. (1996). Epidemiology of cancer. In Oxford textbook of medicine (ed.
D.J.Weatherall, J.G.G. Ledingham, and D.A.Warrell), pp. 197–221. Oxford University
Press, Oxford.
Donohoe, R.T. and Benton, D. (2000). Glucose tolerance predicts performance on tests of
memory and cognition. Physiol. Behav. 71 (3–4), 395–401.
Driutskaia, S.M. and Riabkova,V.A. (2004). Hygienic assessment of iodine deficiency in the
Khabarovsk Territory. [In Russian]. Gig. Sanit. Jul–Aug (4), 15–18.
Eaton, S.B. and Eaton, S.B. (2000). Paleolithic vs. modern diets—selected pathophysiological
implications. Eur. J. Nutr. 39 (2), 67–70.
Eaton, S.B. and Eaton, S.B. III (2003). An evolutionary perspective on human physical activity:
implications for health. Comp. Biochem. Physiol. A 136, 153–9.
205
206
30/9/05
12:27 PM
Page 206
BERNARD GESCH
Eaton, S.B. and Konner, M. (1985). Paleolithic nutrition. A consideration of its nature and
current implications. New Engl. J. Med. 312, 283–9.
Eaton, S.B., Eaton, S.B. III, and Konner, M.J. (1997). Paleolithic nutrition revisited:
a twelve-year retrospective on its nature and implications. Eur. J. Clin. Nutr. 51, 207–16.
Eaton, S.B., Cordain, L., and Lindeberg, S. (2002a). Evolutionary health promotion:
a consideration of common counterarguments. Prev. Med. 34 (2), 119–23.
Eaton, S.B., Strassman, B.I., et al. (2002b). Evolutionary health promotion. Prev. Med. 34, 109–18.
Egger, J., Carter, C.M., Graham, P.J., Gumley, D., and Soothill, J.F. (1985). Controlled trial of
oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1, 540–5.
Ellis, E.F., et al. (1992). Effect of dietary n-3 fatty acids on cerebral microcirculation, Am. J.
Physiol. 258, H1780–H1785.
Eves, A. and Gesch, C.B. (2003). Food provision and the nutritional implications of food choices
made by young adult males in a young offenders’ institution. J. Hum. Nutr. Dietet. 16, 167–79.
FAO (2003). The state of food insecurity in the world. UN Food and Agriculture Organisation Geneva.
FAO/WHO (1994). Expert consultation on the role of dietary fats and oils in human nutrition. FAO,
Rome.
Fenton, W.S., Dickerson, F., Boronow, J., Hibbeln, J.R., and Knable, M. (2001). A placebocontrolled trial of omega-3 fatty acid (ethyl eicosapentaenoic acid) supplementation for residual
symptoms and cognitive impairment in schizophrenia. Am. J. Psychiatry 158 (12), 2071–4.
Fernstrom, J.D. (1999). Effects of dietary polyunsaturated fatty acids on neuronal function. Lipids
34, 161–9.
Flint, R.W. and Turek, C. (2003). Glucose effects on a continuous performance test of
attention in adults. Behav. Brain Res. 142, 217–28.
Foley, R.A. and Lee, P.C. (1991). Ecology and energetics of encephalization in hominid
evolution. Phil.Trans. R. Soc. Lond. B 334, 223–32.
Food and Nutrition Board (2002). Letter report on dietary reference intakes for trans fatty acids.
Drawn from Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein,
and amino acids (macronutrients). National Academies Press,Washington, DC.
Foster, H.G., Hillbrand, M., and Silverstein, M. (1993). Neuropsychological deficit and
aggressive behavior: a prospective study. Prog. Neuropsychopharmacol. Biol. Psychiatry. 17, 939–46.
Gans, D.A., Harper, A.E., Bachorowski, J-A., Newman, J.P., Shrago, E.S., and Taylor, S.
(1990). Sucrose and delinquency: oral sucrose tolerance test and nutritional assesment. Pediatrics
86 (2), 254–62.
Gerrior, S.A. and Zizza, C. (1994). Nutrient content of the U.S. food supply 1909–1990, Home
Economics Research Report No. 52. US Department of Agriculture,Washington, D C.
Gesch, C.B. (2002). A recipe for peace: the role of nutrition in social behaviour. In Foodstuff.
Living in an age of feast and famine (ed. J. Holden, L. Howland, and D. Stedman Jones),
pp. 111–16. DEMOS, London.
Gesch, C.B., Hammond, S.M., Hampson, S.E., Eves, A., and Crowder, M.J. (2002). Influence
of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of
young adult prisoners. Br. J. Psychiatry 181, 22–8.
Giancola, P.R., Mezzich, A.C., and Tarter, R.E. (1998). Executive cognitive functioning,
temperament, and antisocial behavior in conduct-disordered adolescent females. J. Abnorm.
Psychol. 107, 629–41.
Gibbs, C.R., Lip, G.Y., and Beevers, D.G. (2000). Salt and cardiovascular disease: clinical and
epidemiological evidence. J. Cardiovasc. Risk 7, 9–13.
30/9/05
12:27 PM
Page 207
GISSI-Prevenzione Investigators (1999). Dietary supplementation with n-3 polyunsaturated fatty
acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo
Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico. Lancet 354, 447–55.
Golomb, B.A., Stattin, H., and Mednick, S. (2000). Low cholesterol and violent crime.
J. Psychiatr. Res. 34 (4–5), 301–9.
Halas, E.S., Reynolds, G.M., and Sandstead, H.H. (1977). Intra-uterine nutrition and its effects
on aggression. Physiol. Behav. 19, 653–61.
Hamazaki, T., Sawazaki, S., Itomura, M., et al. (1996).The effect of docosahexaenoic acid on
aggression in young adults. J. Clin. Invest. 97, 1129–33.
Hamazaki, T., Sawazaki, S., Nagao,Y., Kuwamori, T.,Yazawa, K., Mizushima,Y., and
Kobayashi, M. (1998). Docosahexaenoic acid does not affect aggression of normal volunteers
under nonstressful conditions. A randomized, placebo-controlled, double-blind study. Lipids 33,
663–7.
Hanas, J.S., Hazuda, D.J., Bogenhagen, D.F., Wu, F.Y., and Wu, C.W. (1983). Xenopus
transcription factor A requires zinc for binding to the 5 S RNA gene. J. Biol. Chem. 258, 14120–5.
Harnack, L., Stang, J., and Story, M. (1999). Soft drink consumption among US children and
adolescents: nutritional consequences. J. Am. Dietet. Assoc. 99, 436–41.
Hartvig, P., Lindner, K.J., Bjurling, P., Laengstrom, B., and Tedroff, J. (1995). Pyridoxine effect
on synthesis rate of serotonin in the monkey brain measured with positron emission
tomography. J. Neural.Transm. Gen. Sect. 102 (2), 91–7.
Harvey, P.H. and Clutton-Brock, T.H. (1985). Life history variation in primates. Evolution 39, 557–81.
Hawkes, W.C. and Hornbostel, L. (1996). Effects of dietary selenium on mood in healthy men
living in a metabolic research unit. Biol. Psychiatry 39 (2), 121–8.
Heiss, L.E. (1995). Changing family patterns in Western Europe: opportunity and risk factors
for adolescent development. In Psychosocial disorders in young people. time, trends and their causes
(ed. M. Rutter and D.J. Smith), pp. 104–93. John Wiley and Sons, New York.
Heseker, H., Kubler, W., Pudel,V., and Westenhofer, J. (1995). Interaction of vitamins with
mental performance. Bibl. Nutr. Dieta. (52), 43–55.
Hibbeln, J.R. (2001). Seafood consumption and homicide mortality. A cross-national ecological
analysis. World Rev. Nutr. Diet 88, 41–6.
Hibbeln, J.R., Umhau, J.C., and Linnoila, M. (1998). A replication study of violent and
nonviolent subjects: cerebrospinal fluid metabolites of serotonin and dopamine are predicted
by plasma essential fatty acids. Biol. Psychiatry 44, 243–9.
Hightower, J.M. and Moore, D. (2003). Mercury levels in high-end consumers of fish. Environ.
Health Perspect. 111 (4), 604–8.
Hirayama, S., et al. (2004). Effect of docosahexaenoic acid-containing food administration on
symptoms of attention-deficit/hyperactivity disorder—a placebo controlled double-blind study.
Eur. J. Clin. Nutr. 58 (3), 467–73.
Holland, B., Welch A.A., Unwin, I.D., et al. (eds.) (1991). McCance and Widdowson’s the
composition of foods, 5th edn. Royal Society of Chemistry and Ministry of Agriculture, Fisheries,
and Food, Cambridge.
Home Office (1997). Criminal statistics for England and Wales (1996). HMSO, London.
Hubbard, P.C. and Lummis, S.C. (2000). Zn(2) enhancement of the recombinant 5-HT(3)
receptor is modulated by divalent cations. Eur. J. Pharmacol. 394 (2–3), 189–97.
Innis, S.M.,Vaghri, Z., and King, D.J. (2004). N-6 Docosapentaenoic acid is not a predictor of
low docosahexaenoic acid in Canadian pre-school children. Am. J. Clin. Nutr. 80, 768–73.
207
208
30/9/05
12:27 PM
Page 208
BERNARD GESCH
Kelley, A.E., Bakshi,V.P., Haber, S.N., Steininger, T.L., Will, M.J., and Zhang, M. (2002).
Opioid modulation of taste hedonics within the ventral striatum. Physiol. Behav. 76 (3), 365–77.
Kershaw, C. (1999). Reconvictions of offenders sentenced or discharged from prison in 1994, England and
Wales, The Home Office Statistics Bulletin 5/99. Research Development and Statistics
Directorate, London.
Kinsbourne, M. (1994). Sugar and the hyperactive child. New Engl. J. Med. 330, 355–6.
Klein, R.G., Avery, G., Cruz-Uribe, K., Halkett, D., Parkington, J.E., Steele, T.,Volman, T.P.,
and Yates, R. (2004).The Ysterfontein 1 Middle Stone Age site, South Africa, and early human
exploitation of coastal resources. Proc. Natl Acad. Sci. USA 101 (16), 5708–15.
Knowler, W.C., et al. (2002). Reduction in the incidence of type 2 diabetes with lifestyle
intervention of metformin. New Engl. J. Med. 346, 393–403.
Koletzko, B. (1992).Trans fatty acids may impair biosynthesis of long-chain polyunsaturates and
growth in man. Acta Paediatr. 81, 302–6.
Konofal, E., Lecendreux, M., Arnulf, I., and Mouren, M.C. (2004). Iron deficiency in children
with attention-deficit/hyperactivity disorder. Arch. Pediatr. Adolesc. Med. 158 (12), 1113–15.
Kris-Etherton, P. et al. (2001). Summary of the scientific conference on dietary fatty acids and
cardiovascular health: conference summary from the nutrition committee of the American
Heart Association. Circulation 103, 1034–9.
Krittayaphong, R., Cascio, W.E., et al. (1997). Heart rate variability in patients with coronary
artery disease: differences in patients with higher and lower depression scores. Psychosom. Med.
59, 231–5.
LaPierre, D., Braun, C.M.J., and Hodgins, S. (1995).Ventral frontal deficits in psychopathy:
neuropsychological test findings. Neuropsychologia 131, 139–51.
Ledger, H.P. (1968). Body composition as a basis for a comparative study of some East African
mammals. In Comparative nutrition of wild animals (ed. M.A. Crawford), pp. 289–310,
Symposiums of the Zoological Society, London, no. 21. Zoological Society, London.
Leonard, W.R. and Robertson, M.L. (1997). Comparative primate energetics and hominid
evolution. Am. J. Phys. Anthropol. 102, 265–81.
Linnoila, M.V.,Virkkunen, M., et al. (1983). Low cerebrospinal fluid 5-hydroxyindoleacetic acid
concentration differentiates impulsive from nonimpulsive violent behavior. Life Sci. 33,
2609–14.
Liu, J., Raine, A.,Venables, P.H., and Mednick, S.A. (2004). Malnutrition at age 3 years and
externalizing behavior problems at ages 8, 11, and 17 years. Am. J. Psychiatry 161 (11), 2005–13.
Ludwig, D.S., Peterson, K.E., and Gortmaker, S.L. (2001). Relation between consumption of
sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 357,
505–8.
Maes, M., D’Haese, P.C., Scharpe, S., D’Hondt, P.D., Cosyns, P., and De Broe, M.E. (1994).
Hypozincemia in depression. J. Affect. Dis. 31, 135–40.
Maes, M.,Vandoolaeghe, E., Neels, H., Demedts, P., Wauters, A., Meltzer, H.Y., Altamura, C.,
and Desnyder, R. (1997). Lower serum zinc in major depression is a sensitive marker of
treatment resistance and of the immune/inflammatory response in that illness. Biol. Psychiatry
42, 349–58.
MAFF (UK Ministry of Agriculture, Fisheries, and Food) (1997). Food surveillance information
sheet, No. 126. Joint Food Safety and Standards Group, MAFF, London.
Manger, M.S., Winichagoon, P., Pongcharoen, T., Gorwachirapan, S., Boonpraderm, A.,
McKenzie, J., and Gibson, R.S. (2004). Multiple micronutrients may lead to improved
cognitive function in NE Thai schoolchildren. Asia Pac. J. Clin. Nutr. 13, 46.
30/9/05
12:27 PM
Page 209
Marshall, E. (2000).The shots heard round the world. Science 289, 570–4.
Martin, R.D. (1983). Human brain evolution in an ecological context, fifty-second James Arthur
Lecture on the Evolution of the Human Brain. American Museum of Natural History,
New York.
Masters, R.D., Coplan, M.J., Hone, B.T., and Dykes J.E. (2000). Association of silicoflouride
treated water with elevated lead. Neurotoxicology 21 (6), 1091–100.
Mayer, A.M. (1997). Historical changes in the mineral content of fruits and vegetables. Br. Food J.
99 (6), 207–211.
McCance, R.A., Widdowson, E.M., and Shackleton, L.R.B. (1936). The nutritive value of fruits,
vegetables and nuts, Medical Research Council Special Report Series No. 213. HMSO, London.
McLoughlin, I.J. and Hodge, J.S. (1990). Zinc in depressive disorder. Acta Psychiatr. Scand. 82,
451–3.
Morgan, E. (1990). The scars of evolution. Oxford University Press, Oxford.
Mulligan, S.J. and MacVicar, B.A. (2004). Calcium transients in astrocyte endfeet cause
cerebrovascular constrictions. Nature 431 (7005), 195–9.
Munro, N. (1987). A three year study of iron deficiency and behavior in rhesus monkeys. Int. J.
Biosoc. Res. 9, 35–62.
Needleman, H.L., Riess, J.A., Tobin, M.J., Biesecker, G.E., and Greenhouse, J.B. (1996). Bone
lead levels and delinquent behaviour. J. Am. Med. Assoc. 275 (5), 363–9.
Nemets, B., Stahl, Z., and Belmaker, R.H. (2002). Addition of omega-3 fatty acid to
maintenance medication treatment for recurrent unipolar depressive disorder. Am. J. Psychiatry
159 (3), 477–9.
Nestle, M. (2002). Big food: politics and nutrition in the United States. In Foodstuff. Living in an
age of feast and famine (ed. J. Holden, L. Howland, and D. Stedman Jones), pp. 83–90. DEMOS,
London.
Nestle, M. (2003).The ironic politics of obesity. Science 299, 781.
Nielsen, F.H. (2000). Evolutionary events culminating in specific minerals becoming essential for
life. Eur. J. Nutr. 39 (2), 62–6.
Nielson, P. and Nachtigall, D. (1998). Iron supplementation in athletes. Current
recommendations. Sports Med. 26, 207–16.
Nowak, G., Siwek, M., Dudek, D., Zieba, A., and Pilc, A. (2003). Effect of zinc
supplementation on antidepressant therapy in unipolar depression: a preliminary
placebo-controlled study. Pol. J. Pharmacol. 55 (6), 1143–7.
O’Dea, K. (1991) Cardiovascular risk factors in Australian aborigines. Clin. Exp. Pharmacol.
Physiol. 18, 85–8.
Oomen, C.M., et al. (2001). Association between trans fatty acid intake and 10-year risk of
coronary heart disease in the Zutphen Elderly Study: a prospective population-based study.
Lancet 357, 746–51.
Oteiza, P.I., Hurley, L., Lonnerdal, B., and Keen, C. (1990). Effects of marginal zinc deficiency
on microtubule polymerization in the developing rat brain. Biol.Trace Elm. Res. 23, 13–23.
Palakurthi, S.S., Flückiger, R., Aktas, H., Changolkar, A.K., Shahsafaei, A., Harneit, S., Kilic, E.,
and Halperin, J.A. (2000). Inhibition of translation initiation mediates the anticancer effect of
the n-3 polyunsaturated fatty acid eicosapentaenoic acid. Cancer Res. 60, 2919–25.
Parkington, J.E. (1998). The impact of the systematic exploitation of marine foods on human evolution.
Colloquia of the Dual Congress of the International Association of the Study of Human
Paleontology and the International Study of Human Biologists, Sun City, South Africa, 28 June
to 4 July, 1998.
209
210
30/9/05
12:27 PM
Page 210
BERNARD GESCH
Peet, M. (2004). International variations in the outcome of schizophrenia and the prevalence of
depression in relation to national dietary practices: an ecological analysis. Br. J. Psychiatry 184,
404–8.
Peet, M. and Horrobin, D.F. (2002). A dose-ranging study of the effects of ethyl-eicosapentaenoate
in patients with ongoing depression despite apparently adequate treatment with standard drugs.
Arch. Gen. Psychiatry 59 (10), 913–19.
Peet, M., Glen, I., and Horrobin, D.F. (eds.) (1999). Phospholipid spectrum disorder in psychiatry.
Marius Press, Carnforth.
Peet, M., Brind, J., Ramchand, C.N., Shah, S., and Vankar, G.K. (2001).Two double-blind
placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia.
Schizophr. Res. 49 (3), 243–51.
Peet, M., Horrobin, D.F.; E-E Multicentre Study Group. (2002). A dose-ranging exploratory
study of the effects of ethyl-eicosapentaenoate in patients with persistent schizophrenic
symptoms. J. Psychiatr. Res. 36 (1), 7–18.
Pennington, B.F. and Bennetto, L. (1993). Main effects of transactions in the neuropsychology of
conduct disorder. Dev. Psychopathol. 5 (1–2), 153–64.
Peppiatt, C. and Attwell, D. (2004). Neurobiology: feeding the brain. Nature 431 (7005), 137–8.
Pine, D.S., Wasserman, G.A., Miller, L., Coplan, J.D., Bagiella, E., Kovelenku, P., Myers, M.M.,
and Sloan, R.P. (1998). Heart period variability and psychopathology in urban boys at risk
for delinquency. Psychophysiology 35 (5), 521–9.
Popkin, B.M., Ge, K., Zhai, F., Xuguang, G., and Ma, H. (1993).The nutritional transition in
China: a cross sectional analysis. Eur. J. Clin. Nutr. 47, 333–46.
Prentice, A. and Jebb, S. (2004). Energy intake/physical activity interactions in the homeostasis of
body weight regulation. Nutr. Rev. 62 (7 Pt, 2), S98–104.
Prynne, C.J., Paul, A.A., Price, G.M., Day, K.C., Hilder, W.S., and Wadsworth, M.E. (1999).
Food and nutrient intake of a national sample of 4-year-old children in 1950, comparison with
the 1990s. Public Health Nutr. 2 (4), 537–47.
Puri, B.K. and Richardson, A.J. (1998). Sustained remission of positive and negative symptoms
of schizophrenia following treatment with eicosapentaenoic acid. Arch. Gen. Psychiatry 55 (2), 188–9.
Puri, B.K., Richardson, A.J., Horrobin, D.F., Easton, T., Saeed, N., Oatridge, A., et al. (2000).
Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission,
normalisation of blood fatty acids, reduced neuronal membrane phospholipid turnover and
structural brain changes. Int. J. Clin. Pract. 54 (1), 57–63.
Puri, B.K., Counsell, S.J., Hamilton, G., Richardson, A.J., and Horrobin, D.F. (2001).
Eicosapentaenoic acid in treatment-resistant depression associated with symptom remission,
structural brain changes and reduced neuronal phospholipid turnover. Int. J. Clin. Pract. 55 (8),
560–3.
Puri, B.K., Counsell, S.J., Richardson, A.J., and Horrobin, D.F. (2002). Eicosapentaenoic acid
in treatment-resistant depression. Arch. Gen. Psychiatry 59 (1), 91–2.
Raine, A.,Venables, P.H., et al. (1995). High autonomic arousal and electrodermal orienting at
age 15 years as protective factors against criminal behavior at age 29 years. Am. J. Psychiatry
152 (11), 1595–600.
Raine, A., Mellingen, K., Liu, J.,Venables, P., and Mednick, S.A. (2003). Effects of
environmental enrichment at ages 3–5 years on schizotypal personality and antisocial behavior
at ages 17 and 23 years. Am. J. Psychiatry 160, 1627–35.
Redmer, D.A., Wallace, J.M., and Reynolds, L.P. (2004). Effect of nutrient intake during
pregnancy on fetal and placental growth and vascular development. Domest. Anim. Endocrinol.
27 (3), 199–217.
30/9/05
12:27 PM
Page 211
Richardson, A.J. and Puri, B.K. (2000).The potential role of fatty acids in attentiondeficit/hyperactivity disorder. Prostaglandins Leukot. Essent. Fatty Acids 63 (1–2), 79–87.
Richardson, A.J. and Puri, B.K. (2002). A randomized double-blind, placebo-controlled study of
the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms
in children with specific learning difficulties. Prog. Neuropsychopharmacol. Biol. Psychiatry 26 (2),
233–9.
Richardson, A.J. and Ross, M.A. (2000). Fatty acid metabolism in neurodevelopmental
disorder: a new perspective on associations between attention-deficit/hyperactivity
disorder, dyslexia, dyspraxia and the autistic spectrum. Prostaglandins Leukot. Essent. Fatty Acids
63 (1–2), 1–9.
Richardson, A.J., Easton, T., and Puri, B.K. (2000). Red cell and plasma fatty acid changes
accompanying symptom remission in a patient with schizophrenia treated with
eicosapentaenoic acid. Eur. Neuropsychopharmacol. 10 (3), 189–93.
Rightmire, G.P. and Deacon, H.J. (1991). Comparative studies of Late Pleistocene human
remains from Klasies River Mouth, South Africa. J. Hum. Evol. 20, 131–56.
Rubia, K., Oosterlaan, J., Sergeant, J., Brandeis, D., and van Leeuwen, T. (1998). Inhibitory
dysfunction in hyperactive boys. Behav. Brain Res. 94 (1), 25–32.
Rutter, M., Giller, H., and Hagell, H. (1998). Antisocial behaviour by young people. Cambridge
University Press, Cambridge.
Sazawal, S., Black, R.E., Menon,V.P., Dinghra, P., Caulfield, L.E., Dhingra, U., and Bagati, A.
(2001). Zinc supplementation in infants born small for gestational age reduces mortality: a
prospective, randomized, controlled trial. Pediatrics 108 (6), 1280–6.
Schab, D.W. and Trinh, N.H. (2004). Do artificial food colors promote hyperactivity in children
with hyperactive syndromes? A meta-analysis of double-blind placebo-controlled trials. J. Dev.
Behav. Pediatr. 25 (6), 423–34.
Schauss, A.G. (1978). Differential outcomes among probationers comparing orthomolecular
approaches to conventional casework/counselling. J. Orthomol. Psychiatry 8 (3), 158–68.
Schoenthaler, S.J. (1983).The Northern California diet and Behaviour Program: an empirical
examination of 3000 incarcerated juveniles in Stanilaus County Juvenile Hall. Int. J. Biosoc. Res.
5 (2), 99–106.
Schoenthaler, S.J. (1994). Sugar and children’s behavior. New Engl. J. Med. 330 (26), 1901–4.
Schoenthaler, S.J. and Bier, I.D. (2000). The effect of vitamin and mineral supplementation
juvenile delinquency among American schoolchildren: a randomised double blind placebo
controlled study. J. Altern. Complement. Med. 6 (1), 7–17.
Schoenthaler, S.J., Amos, S., Doraz, W., et al. (1997).The effect of randomised vitamin-mineral
supplementation on violent and non-violent antisocial behavior among incarcerated juveniles.
J. Nutr. Environ. Med. 7, 343–52.
Schrauzer, G.N. (2002). Lithium: occurrence, dietary intakes, nutritional essentiality. J. Am. Coll.
Nutr. 21 (1), 14–21.
Shepherd, J.T., Abboud, F.M., and Geiger, S.R. (eds.) (1983). Handbook of physiology. Section 2,
Vol. 3. Cardiovascular system. American Physiological Society, Bethesda, Maryland.
Sherman, L., et al. (1997). Preventing crime: what works, what doesn’t, what’s promising, a report
to the United States Congress, prepared for the National Institute of Justice.
Shipman, P. and Walker, A. (1989).The costs of becoming a predator. J. Hum. Evol. 18, 373–92.
Short, C. (2002).The rich diet, and the poor go hungry. In: Foodstuff. Living in an age of feast and
famine (ed. J. Holden, L. Howland, and D. Stedman Jones), pp. 131–7. DEMOS, London.
Shreeve, J. (1995). The Neandertal enigma: solving the mystery of modern human origins.William
Morrow, New York.
211
212
30/9/05
12:27 PM
Page 212
BERNARD GESCH
Simopoulos, A.P. and Pavlow, K.N. (eds.) (2001). Nutrition and fitness: diet, genes, physical
activity and health, Proceedings of 4th International Conference on Nutrition and Fitness,
Athens, May (2000). World Rev. Nutr. Diet. 89.
Smith, D.J. (1995).Youth crime and conduct disorders: trends, patterns and causal explanations.
In Psychosocial disorders in young people. time, trends and their causes (ed. M. Rutter and D.J. Smith),
pp. 389–489. John Wiley and Sons, New York.
Stacey, M., Curnow, R.N., and Ward, N. (1994). Analyzing the relationship between reading
ability and the concentrations of trace elements in hair and saliva. J. Nutr. Med. 4, 25–31.
Stanley, B., Molcho, A, Stanley, M., Winchel, R., Gameroff, M.J., Parsons, B., and Mann J.J.
(2000). Association of aggressive behavior with altered serotonergic function in patients who
are not suicidal. Am. J. Psychiatry 157 (4), 609–14.
Stevens, L.J., Zentall, S.S., and Abate, M.L. (1996). Omega-3 fatty acids in boys with behavior,
learning, and health problems. Physiol. Behav. 59, 915–20.
Stevens, L., Zhang, W., Peck, L., Kuczek, T., Grevstad, N., Mahon, A., Zentall, S.S.,
Arnold, L.E., and Burgess, J.R. (2003). EFA supplementation in children with
inattention, hyperactivity, and other disruptive behaviors. Lipids 38 (10), 1007–21.
Stoll, A.L., Severus, W.E., Freeman, M.P., Rueter, S., Zboyan, H.A., Diamond, E., et al.
(1999). Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled
trial. Arch. Gen. Psychiatry 56 (5), 407–12.
Stoney, C.M. and Engebretson T.O. (2000). Plasma homocysteine concentrations are positively
associated with hostility and anger. Life Sci. 66 (23), 2267–75.
Stretesky, P.B. and Lynch, M.J. (2001).The relationship between lead exposure and homicide.
Arch. Pediatr. Adolesc. Med. 155 (5), 579–82.
Stringer, C. (2000). Palaeoanthropology. Coasting out of Africa. Nature 405 (6782), 24–5, 27.
Stynder, D.D., Moggi-Cecchi, J., Berger, L.R., and Parkington, J.E. (2001). Human
mandibular incisors from the late Middle Pleistocene locality of Hoedjiespunt 1, South Africa.
J. Hum. Evol. 41 (5), 369–83.
Tanzer, F.,Yaylaci, G., Ustdal, M., and Yonem, O. (2004). Serum zinc level and its effect on
anthropometric measurements in 7–11 year-old children with different socioeconomic
backgrounds. Int. J.Vitamin Nutr. Res. 74 (1), 52–6.
Taylor, E. (1998). Clinical foundations of hyperactivity research. Behav. Brain Res. 94 (1), 11–24.
Taylor, M.J., Carney, S., Geddes, J., and Goodwin, G. (2003). Folate for depressive disorders.
Cochrane Database Syst. Rev. (02) CD003390.
Thomson, G.O.B., Raab, G.M., Hepburn, W.S., Hunter, R., Fulton, M., and Laxen, D.P.H.
(1989). Blood lead levels and children’s behaviour—results from the Edinburgh lead study.
J. Child Psychol. Psychiatry 30, 515–28.
Tobias, P.V. (2002). Some aspects of the multifaceted dependence of early humanity on water.
Nutr. Health 16 (1), 13–17.
Tordoff, M.G. and Alleva, A.M. (1990). Effect of drinking soda sweetened with aspartame or
high-fructose corn syrup on food intake and body weight. Am. J. Clin. Nutr. 51, 963–9.
Tulen, J.H., Bruijn, J.A., et al. (1996) Anxiety and autonomic regulation in major depressive
disorder: an exploratory study. J Affect Disord. 40, 61–71.
Tuomilehto, J., et al. (2002). Prevention of type 2 diabetes mellitus by changes in lifestyle among
subjects with impaired glucose tolerance. New Engl. J. Med. 344, 1343–50.
Uauy, R., Hoffman, D.R., Peirano, P., Birch, D.G., and Birch, E.E. (2001). Essential fatty acids
in visual and brain development. Lipids 36 (9), 885–95.
30/9/05
12:27 PM
Page 213
US Department of Health and Human Services (1996). Physical activity and health: a report of the
Surgeon General, pp. 85–172. Centers for Disease Control and Prevention, Atlanta, Georgia.
Vallee, B.L. and Falchuk, K.H. (1981). Zinc and gene expression. Philos.Trans. R. Soc. Lond.
B Biol. Sci. 294, 185–97.
van Houwelingen, A.C. and Hornstra, G. (1994).Trans fatty acids in early human development.
World Rev. Nutr. Diet. 75, 175–8.
Virkkunen, M.E., Horrobin, D.F., Jenkins, D.K., and Manuku, M.S. (1987). Plasma
phospholipids, essential fatty acids and prostaglandins in alcoholic, habitually violent and
impulsive offenders. Biol. Psychiatry 22, 1087–96.
Virkkunen, M., Goldman, D., et al. (1995). Low brain serotonin turnover rate (low CSF
5-HIAA) and impulsive violence. J. Psychiatry Neurosci. 20, 271–5.
Voigt, R.G., Llorente, A.M., Jensen, C.L., Fraley, J.K., Berretta, M.C., and Heird, W.C.
(2001). A randomized, double-blind, placebo-controlled trial of docosahexaenoic acid
supplementation in children with attention-deficit/hyperactivity disorder. J. Pediatr. 139 (2),
189–96.
Wadsworth, M.E.J. (1976). Delinquency, pulse rates and early emotional deprivation, Br. J.
Criminol. 16 (3), 245–56.
Walsh, W.J., Isaacson, H.R., Rehman, F., and Hall, A. (1997). Elevated blood copper/zinc
ratios in assaultive young males. Physiol. Behav. 62, 327–9.
Walsh, W.J., Glab, L.B., and Haakenson, M.L. (2004). Reduced violent behavior following
biochemical therapy. Physiol. Behav. 82 (5), 835–9.
Wang,Y., Crawford, M.A., Chen, J., Li, J., Ghebremeskel, K., Campbell, C., Fan, W., Parker, R.,
and Leyton, J. (2003). Fish consumption, blood docosahexaenoic acid and chronic diseases in
Chinese rural populations. Comp. Biochem. Physiol. A Mol. Integr. Physiol. 136 (1),127–40.
Ward, N.I., Durrant, S., Sankey, R.J., Bound, J.P., and Bryce-Smith, D. (1990). Elemental
factors in human fetal development. J. Nutr. Med. 1, 19–26.
Wauben, I.P., Xing, H.C., and Wainwright, P.E. (1999). Neonatal dietary zinc deficiency in
artificially reared rat pups retards behavioral development and interacts with essential fatty acid
deficiency to alter liver and brain fatty acid composition. J. Nutr. 129 (10), 1773–81.
WHO (1998). Obesity: preventing and managing the global epidemic,WHO Technical Report. Series
894, pp. 1–276.World Health Organization, Geneva.
WHO (2000). A global agenda for combating malnutrition: progress report,WHO/NHD/00.6.World
Health Organization, Geneva.
WHO (2002). Programming of chronic disease by impaired fetal nutrition: evidence and implications for
policy and intervention strategies, documents WHO/NHD/02.3 and WHO/NPH/02.1.World
Health Organization, Geneva.
WHO (2003). Diet, nutrition and the prevention of chronic disease, Report of a Joint FAO/WHO
Expert Consultation,Technical report Series 916.World Health Organization, Geneva.
WHO/UNICEF (1995). Global prevalence of vitamin A deficiency, MDIS Working Paper No. 2,
document WHO/NUT/95.3.World Health Organization, Geneva.
WHO/UNICEF/International Council for the Control of Iodine Deficiency Disorders
(1999). Progress towards the elimination of iodine deficiency disorders (IDD), document
WHO/NHD/99.4.World Health Organization, Geneva.
WHO/UNICEF/United Nations University (2001). Iron deficiency anaemia assessment, prevention
and control: a guide for programme managers, document WHO/NHD/01.3.World Health
Organization, Geneva.
213
30/9/05
12:27 PM
Page 214
Willet, M.C. (1995). Diet, nutrition, and avoidable cancer. Environ. Health Perspect. 103 (Suppl. 8),
165–70.
Willett, W.C., et al. (1993). Intake of trans fatty acids and risk of coronary heart disease among
women. Lancet 341, 581–5.
Wolraich, M.L., Lindgren, S.D., Stumbo, P.J., Stegink, L.D., Appelbaum, M.I., and Kiritsy, M.C.
(1994). Effects of diets high in sucrose or aspartame on the behavior and cognitive performance of
children. New Engl. J. Med. 330 (5), 301–7.
World Cancer Research Fund in association with American Institute for Cancer Research
(1997). Food, nutrition and the prevention of cancer: a global perspective. American Institute for Cancer
Research,Washington, DC.
Zanarini, M.C. and Frankenburg, F.R. (2003). Omega-3 fatty acid treatment of women with
borderline personality disorder: a double-blind, placebo-controlled pilot study. Am. J. Psychiatry 160
(1), 167–9.
Zhang, M. and Kelley, A.E. (2000). Enhanced intake of high-fat food following striatal mu-opioid
stimulation: microinjection mapping and fos expression. Neuroscience 99 (2), 267–77.

Bernard Gesch is a senior research scientist in the

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